---
_id: '15033'
abstract:
- lang: eng
text: The GNOM (GN) Guanine nucleotide Exchange Factor for ARF small GTPases (ARF-GEF)
is among the best studied trafficking regulators in plants, playing crucial and
unique developmental roles in patterning and polarity. The current models place
GN at the Golgi apparatus (GA), where it mediates secretion/recycling, and at
the plasma membrane (PM) presumably contributing to clathrin-mediated endocytosis
(CME). The mechanistic basis of the developmental function of GN, distinct from
the other ARF-GEFs including its closest homologue GNOM-LIKE1 (GNL1), remains
elusive. Insights from this study largely extend the current notions of GN function.
We show that GN, but not GNL1, localizes to the cell periphery at long-lived structures
distinct from clathrin-coated pits, while CME and secretion proceed normally in
gn knockouts. The functional GN mutant variant GNfewerroots,
absent from the GA, suggests that the cell periphery is the major site of GN action
responsible for its developmental function. Following inhibition by Brefeldin
A, GN, but not GNL1, relocates to the PM likely on exocytic vesicles, suggesting
selective molecular associations en route to the cell periphery. A study of GN-GNL1
chimeric ARF-GEFs indicates that all GN domains contribute to the specific GN
function in a partially redundant manner. Together, this study offers significant
steps toward the elucidation of the mechanism underlying unique cellular and development
functions of GNOM.
acknowledgement: "The authors would like to gratefully acknowledge Dr Xixi Zhang for
cloning the GNL1/pDONR221 construct and for useful discussions.H2020 European Research\r\nCouncil
Advanced Grant ETAP742985 to Jiří Friml, Austrian Science Fund I 3630-B25 to Jiří
Friml"
article_processing_charge: Yes
article_type: original
author:
- first_name: Maciek
full_name: Adamowski, Maciek
id: 45F536D2-F248-11E8-B48F-1D18A9856A87
last_name: Adamowski
orcid: 0000-0001-6463-5257
- first_name: Ivana
full_name: Matijevic, Ivana
id: 83c17ce3-15b2-11ec-abd3-f486545870bd
last_name: Matijevic
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
citation:
ama: Adamowski M, Matijevic I, Friml J. Developmental patterning function of GNOM
ARF-GEF mediated from the cell periphery. eLife. 2024;13. doi:10.7554/elife.68993
apa: Adamowski, M., Matijevic, I., & Friml, J. (2024). Developmental patterning
function of GNOM ARF-GEF mediated from the cell periphery. ELife. eLife
Sciences Publications. https://doi.org/10.7554/elife.68993
chicago: Adamowski, Maciek, Ivana Matijevic, and Jiří Friml. “Developmental Patterning
Function of GNOM ARF-GEF Mediated from the Cell Periphery.” ELife. eLife
Sciences Publications, 2024. https://doi.org/10.7554/elife.68993.
ieee: M. Adamowski, I. Matijevic, and J. Friml, “Developmental patterning function
of GNOM ARF-GEF mediated from the cell periphery,” eLife, vol. 13. eLife
Sciences Publications, 2024.
ista: Adamowski M, Matijevic I, Friml J. 2024. Developmental patterning function
of GNOM ARF-GEF mediated from the cell periphery. eLife. 13.
mla: Adamowski, Maciek, et al. “Developmental Patterning Function of GNOM ARF-GEF
Mediated from the Cell Periphery.” ELife, vol. 13, eLife Sciences Publications,
2024, doi:10.7554/elife.68993.
short: M. Adamowski, I. Matijevic, J. Friml, ELife 13 (2024).
date_created: 2024-02-27T07:10:11Z
date_published: 2024-02-21T00:00:00Z
date_updated: 2024-02-28T12:29:43Z
day: '21'
ddc:
- '580'
department:
- _id: JiFr
doi: 10.7554/elife.68993
ec_funded: 1
has_accepted_license: '1'
intvolume: ' 13'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
main_file_link:
- open_access: '1'
url: https://doi.org/10.7554/eLife.68993
month: '02'
oa: 1
oa_version: Published Version
project:
- _id: 261099A6-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742985'
name: Tracing Evolution of Auxin Transport and Polarity in Plants
- _id: 26538374-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I03630
name: Molecular mechanisms of endocytic cargo recognition in plants
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: epub_ahead
publisher: eLife Sciences Publications
quality_controlled: '1'
status: public
title: Developmental patterning function of GNOM ARF-GEF mediated from the cell periphery
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 13
year: '2024'
...
---
_id: '14683'
abstract:
- lang: eng
text: "Mosaic analysis with double markers (MADM) technology enables the generation
of genetic mosaic tissue in mice and high-resolution phenotyping at the individual
cell level. Here, we present a protocol for isolating MADM-labeled cells with
high yield for downstream molecular analyses using fluorescence-activated cell
sorting (FACS). We describe steps for generating MADM-labeled mice, perfusion,
single-cell suspension, and debris removal. We then detail procedures for cell
sorting by FACS and downstream analysis. This protocol is suitable for embryonic
to adult mice.\r\nFor complete details on the use and execution of this protocol,
please refer to Contreras et al. (2021).1"
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: This research was supported by the Scientific Service Units (SSU)
at IST Austria through resources provided by the Imaging & Optics Facility (IOF)
and Preclinical Facilities (PCF). N.A. received support from FWF Firnberg-Programme
(T 1031). G.C. received support from the European Union’s Horizon 2020 research
and innovation programme under the Marie Skłodowska-Curie grant agreement no. 754411
as an ISTplus postdoctoral fellow. This work was also supported by IST Austria institutional
funds, FWF SFB F78 to S.H., and the European Research Council (ERC) under the European
Union’s Horizon 2020 research and innovation programme (grant agreement no. 725780
LinPro) to S.H.
article_number: '102771'
article_processing_charge: No
article_type: review
author:
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Giselle T
full_name: Cheung, Giselle T
id: 471195F6-F248-11E8-B48F-1D18A9856A87
last_name: Cheung
orcid: 0000-0001-8457-2572
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Amberg N, Cheung GT, Hippenmeyer S. Protocol for sorting cells from mouse brains
labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols.
2023;5(1). doi:10.1016/j.xpro.2023.102771
apa: Amberg, N., Cheung, G. T., & Hippenmeyer, S. (2023). Protocol for sorting
cells from mouse brains labeled with mosaic analysis with double markers by flow
cytometry. STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2023.102771
chicago: Amberg, Nicole, Giselle T Cheung, and Simon Hippenmeyer. “Protocol for
Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers
by Flow Cytometry.” STAR Protocols. Elsevier, 2023. https://doi.org/10.1016/j.xpro.2023.102771.
ieee: N. Amberg, G. T. Cheung, and S. Hippenmeyer, “Protocol for sorting cells from
mouse brains labeled with mosaic analysis with double markers by flow cytometry,”
STAR Protocols, vol. 5, no. 1. Elsevier, 2023.
ista: Amberg N, Cheung GT, Hippenmeyer S. 2023. Protocol for sorting cells from
mouse brains labeled with mosaic analysis with double markers by flow cytometry.
STAR Protocols. 5(1), 102771.
mla: Amberg, Nicole, et al. “Protocol for Sorting Cells from Mouse Brains Labeled
with Mosaic Analysis with Double Markers by Flow Cytometry.” STAR Protocols,
vol. 5, no. 1, 102771, Elsevier, 2023, doi:10.1016/j.xpro.2023.102771.
short: N. Amberg, G.T. Cheung, S. Hippenmeyer, STAR Protocols 5 (2023).
date_created: 2023-12-13T11:48:05Z
date_published: 2023-12-08T00:00:00Z
date_updated: 2023-12-18T08:06:14Z
day: '08'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.xpro.2023.102771
ec_funded: 1
external_id:
pmid:
- '38070137'
intvolume: ' 5'
issue: '1'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.xpro.2023.102771
month: '12'
oa: 1
oa_version: Submitted Version
pmid: 1
project:
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: STAR Protocols
publication_identifier:
issn:
- 2666-1667
publication_status: epub_ahead
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Protocol for sorting cells from mouse brains labeled with mosaic analysis with
double markers by flow cytometry
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2023'
...
---
_id: '14274'
abstract:
- lang: eng
text: Immune responses rely on the rapid and coordinated migration of leukocytes.
Whereas it is well established that single-cell migration is often guided by gradients
of chemokines and other chemoattractants, it remains poorly understood how these
gradients are generated, maintained, and modulated. By combining experimental
data with theory on leukocyte chemotaxis guided by the G protein–coupled receptor
(GPCR) CCR7, we demonstrate that in addition to its role as the sensory receptor
that steers migration, CCR7 also acts as a generator and a modulator of chemotactic
gradients. Upon exposure to the CCR7 ligand CCL19, dendritic cells (DCs) effectively
internalize the receptor and ligand as part of the canonical GPCR desensitization
response. We show that CCR7 internalization also acts as an effective sink for
the chemoattractant, dynamically shaping the spatiotemporal distribution of the
chemokine. This mechanism drives complex collective migration patterns, enabling
DCs to create or sharpen chemotactic gradients. We further show that these self-generated
gradients can sustain the long-range guidance of DCs, adapt collective migration
patterns to the size and geometry of the environment, and provide a guidance cue
for other comigrating cells. Such a dual role of CCR7 as a GPCR that both senses
and consumes its ligand can thus provide a novel mode of cellular self-organization.
acknowledgement: "We thank I. de Vries and the Scientific Service Units (Life Sciences,
Bioimaging, Nanofabrication, Preclinical and Miba Machine Shop) of the Institute
of Science and Technology Austria for excellent support, as well as all the rotation
students assisting in the laboratory work (B. Zens, H. Schön, and D. Babic).\r\nThis
work was supported by grants from the European Research Council under the European
Union’s Horizon 2020 research to M.S. (grant agreement no. 724373) and to E.H. (grant
agreement no. 851288), and a grant by the Austrian Science Fund (DK Nanocell W1250-B20)
to M.S. J.A. was supported by the Jenny and Antti Wihuri Foundation and Research
Council of Finland's Flagship Programme InFLAMES (decision number: 357910). M.C.U.
was supported by the European Union’s Horizon 2020 research and innovation programme
under the Marie Skłodowska-Curie grant agreement no. 754411."
article_number: adc9584
article_processing_charge: No
article_type: original
author:
- first_name: Jonna H
full_name: Alanko, Jonna H
id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87
last_name: Alanko
orcid: 0000-0002-7698-3061
- first_name: Mehmet C
full_name: Ucar, Mehmet C
id: 50B2A802-6007-11E9-A42B-EB23E6697425
last_name: Ucar
orcid: 0000-0003-0506-4217
- first_name: Nikola
full_name: Canigova, Nikola
id: 3795523E-F248-11E8-B48F-1D18A9856A87
last_name: Canigova
orcid: 0000-0002-8518-5926
- first_name: Julian A
full_name: Stopp, Julian A
id: 489E3F00-F248-11E8-B48F-1D18A9856A87
last_name: Stopp
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Alanko JH, Ucar MC, Canigova N, et al. CCR7 acts as both a sensor and a sink
for CCL19 to coordinate collective leukocyte migration. Science Immunology.
2023;8(87). doi:10.1126/sciimmunol.adc9584
apa: Alanko, J. H., Ucar, M. C., Canigova, N., Stopp, J. A., Schwarz, J., Merrin,
J., … Sixt, M. K. (2023). CCR7 acts as both a sensor and a sink for CCL19 to coordinate
collective leukocyte migration. Science Immunology. American Association
for the Advancement of Science. https://doi.org/10.1126/sciimmunol.adc9584
chicago: Alanko, Jonna H, Mehmet C Ucar, Nikola Canigova, Julian A Stopp, Jan Schwarz,
Jack Merrin, Edouard B Hannezo, and Michael K Sixt. “CCR7 Acts as Both a Sensor
and a Sink for CCL19 to Coordinate Collective Leukocyte Migration.” Science
Immunology. American Association for the Advancement of Science, 2023. https://doi.org/10.1126/sciimmunol.adc9584.
ieee: J. H. Alanko et al., “CCR7 acts as both a sensor and a sink for CCL19
to coordinate collective leukocyte migration,” Science Immunology, vol.
8, no. 87. American Association for the Advancement of Science, 2023.
ista: Alanko JH, Ucar MC, Canigova N, Stopp JA, Schwarz J, Merrin J, Hannezo EB,
Sixt MK. 2023. CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective
leukocyte migration. Science Immunology. 8(87), adc9584.
mla: Alanko, Jonna H., et al. “CCR7 Acts as Both a Sensor and a Sink for CCL19 to
Coordinate Collective Leukocyte Migration.” Science Immunology, vol. 8,
no. 87, adc9584, American Association for the Advancement of Science, 2023, doi:10.1126/sciimmunol.adc9584.
short: J.H. Alanko, M.C. Ucar, N. Canigova, J.A. Stopp, J. Schwarz, J. Merrin, E.B.
Hannezo, M.K. Sixt, Science Immunology 8 (2023).
date_created: 2023-09-06T08:07:51Z
date_published: 2023-09-01T00:00:00Z
date_updated: 2023-12-21T14:30:01Z
day: '01'
department:
- _id: MiSi
- _id: EdHa
- _id: NanoFab
doi: 10.1126/sciimmunol.adc9584
ec_funded: 1
external_id:
isi:
- '001062110600003'
pmid:
- '37656776'
intvolume: ' 8'
isi: 1
issue: '87'
keyword:
- General Medicine
- Immunology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1126/sciimmunol.adc9584
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
- _id: 05943252-7A3F-11EA-A408-12923DDC885E
call_identifier: H2020
grant_number: '851288'
name: Design Principles of Branching Morphogenesis
- _id: 265E2996-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W01250-B20
name: Nano-Analytics of Cellular Systems
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
publication: Science Immunology
publication_identifier:
issn:
- 2470-9468
publication_status: published
publisher: American Association for the Advancement of Science
quality_controlled: '1'
related_material:
record:
- id: '14279'
relation: research_data
status: public
- id: '14697'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte
migration
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2023'
...
---
_id: '10812'
abstract:
- lang: eng
text: Several promising strategies based on combining or cycling different antibiotics
have been proposed to increase efficacy and counteract resistance evolution, but
we still lack a deep understanding of the physiological responses and genetic
mechanisms that underlie antibiotic interactions and the clinical applicability
of these strategies. In antibiotic-exposed bacteria, the combined effects of physiological
stress responses and emerging resistance mutations (occurring at different time
scales) generate complex and often unpredictable dynamics. In this Review, we
present our current understanding of bacterial cell physiology and genetics of
responses to antibiotics. We emphasize recently discovered mechanisms of synergistic
and antagonistic drug interactions, hysteresis in temporal interactions between
antibiotics that arise from microbial physiology and interactions between antibiotics
and resistance mutations that can cause collateral sensitivity or cross-resistance.
We discuss possible connections between the different phenomena and indicate relevant
research directions. A better and more unified understanding of drug and genetic
interactions is likely to advance antibiotic therapy.
acknowledgement: The authors thank B. Kavčič and H. Schulenburg for constructive feedback
on the manuscript.
article_processing_charge: No
article_type: review
author:
- first_name: Roderich
full_name: Römhild, Roderich
id: 68E56E44-62B0-11EA-B963-444F3DDC885E
last_name: Römhild
orcid: 0000-0001-9480-5261
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Dan I.
full_name: Andersson, Dan I.
last_name: Andersson
citation:
ama: Römhild R, Bollenbach MT, Andersson DI. The physiology and genetics of bacterial
responses to antibiotic combinations. Nature Reviews Microbiology. 2022;20:478-490.
doi:10.1038/s41579-022-00700-5
apa: Römhild, R., Bollenbach, M. T., & Andersson, D. I. (2022). The physiology
and genetics of bacterial responses to antibiotic combinations. Nature Reviews
Microbiology. Springer Nature. https://doi.org/10.1038/s41579-022-00700-5
chicago: Römhild, Roderich, Mark Tobias Bollenbach, and Dan I. Andersson. “The Physiology
and Genetics of Bacterial Responses to Antibiotic Combinations.” Nature Reviews
Microbiology. Springer Nature, 2022. https://doi.org/10.1038/s41579-022-00700-5.
ieee: R. Römhild, M. T. Bollenbach, and D. I. Andersson, “The physiology and genetics
of bacterial responses to antibiotic combinations,” Nature Reviews Microbiology,
vol. 20. Springer Nature, pp. 478–490, 2022.
ista: Römhild R, Bollenbach MT, Andersson DI. 2022. The physiology and genetics
of bacterial responses to antibiotic combinations. Nature Reviews Microbiology.
20, 478–490.
mla: Römhild, Roderich, et al. “The Physiology and Genetics of Bacterial Responses
to Antibiotic Combinations.” Nature Reviews Microbiology, vol. 20, Springer
Nature, 2022, pp. 478–90, doi:10.1038/s41579-022-00700-5.
short: R. Römhild, M.T. Bollenbach, D.I. Andersson, Nature Reviews Microbiology
20 (2022) 478–490.
date_created: 2022-03-04T04:33:49Z
date_published: 2022-08-01T00:00:00Z
date_updated: 2023-08-02T14:41:44Z
day: '01'
department:
- _id: CaGu
doi: 10.1038/s41579-022-00700-5
external_id:
isi:
- '000763891900001'
pmid:
- '35241807'
intvolume: ' 20'
isi: 1
keyword:
- General Immunology and Microbiology
- Microbiology
- Infectious Diseases
language:
- iso: eng
month: '08'
oa_version: None
page: 478-490
pmid: 1
publication: Nature Reviews Microbiology
publication_identifier:
eissn:
- 1740-1534
issn:
- 1740-1526
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: The physiology and genetics of bacterial responses to antibiotic combinations
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 20
year: '2022'
...
---
_id: '11447'
abstract:
- lang: eng
text: Empirical essays of fitness landscapes suggest that they may be rugged, that
is having multiple fitness peaks. Such fitness landscapes, those that have multiple
peaks, necessarily have special local structures, called reciprocal sign epistasis
(Poelwijk et al. in J Theor Biol 272:141–144, 2011). Here, we investigate the
quantitative relationship between the number of fitness peaks and the number of
reciprocal sign epistatic interactions. Previously, it has been shown (Poelwijk
et al. in J Theor Biol 272:141–144, 2011) that pairwise reciprocal sign epistasis
is a necessary but not sufficient condition for the existence of multiple peaks.
Applying discrete Morse theory, which to our knowledge has never been used in
this context, we extend this result by giving the minimal number of reciprocal
sign epistatic interactions required to create a given number of peaks.
acknowledgement: We are grateful to Herbert Edelsbrunner and Jeferson Zapata for helpful
discussions. Open access funding provided by Austrian Science Fund (FWF). Partially
supported by the ERC Consolidator (771209–CharFL) and the FWF Austrian Science Fund
(I5127-B) grants to FAK.
article_number: '74'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Raimundo J
full_name: Saona Urmeneta, Raimundo J
id: BD1DF4C4-D767-11E9-B658-BC13E6697425
last_name: Saona Urmeneta
orcid: 0000-0001-5103-038X
- first_name: Fyodor
full_name: Kondrashov, Fyodor
id: 44FDEF62-F248-11E8-B48F-1D18A9856A87
last_name: Kondrashov
orcid: 0000-0001-8243-4694
- first_name: Kseniia
full_name: Khudiakova, Kseniia
id: 4E6DC800-AE37-11E9-AC72-31CAE5697425
last_name: Khudiakova
orcid: 0000-0002-6246-1465
citation:
ama: Saona Urmeneta RJ, Kondrashov F, Khudiakova K. Relation between the number
of peaks and the number of reciprocal sign epistatic interactions. Bulletin
of Mathematical Biology. 2022;84(8). doi:10.1007/s11538-022-01029-z
apa: Saona Urmeneta, R. J., Kondrashov, F., & Khudiakova, K. (2022). Relation
between the number of peaks and the number of reciprocal sign epistatic interactions.
Bulletin of Mathematical Biology. Springer Nature. https://doi.org/10.1007/s11538-022-01029-z
chicago: Saona Urmeneta, Raimundo J, Fyodor Kondrashov, and Kseniia Khudiakova.
“Relation between the Number of Peaks and the Number of Reciprocal Sign Epistatic
Interactions.” Bulletin of Mathematical Biology. Springer Nature, 2022.
https://doi.org/10.1007/s11538-022-01029-z.
ieee: R. J. Saona Urmeneta, F. Kondrashov, and K. Khudiakova, “Relation between
the number of peaks and the number of reciprocal sign epistatic interactions,”
Bulletin of Mathematical Biology, vol. 84, no. 8. Springer Nature, 2022.
ista: Saona Urmeneta RJ, Kondrashov F, Khudiakova K. 2022. Relation between the
number of peaks and the number of reciprocal sign epistatic interactions. Bulletin
of Mathematical Biology. 84(8), 74.
mla: Saona Urmeneta, Raimundo J., et al. “Relation between the Number of Peaks and
the Number of Reciprocal Sign Epistatic Interactions.” Bulletin of Mathematical
Biology, vol. 84, no. 8, 74, Springer Nature, 2022, doi:10.1007/s11538-022-01029-z.
short: R.J. Saona Urmeneta, F. Kondrashov, K. Khudiakova, Bulletin of Mathematical
Biology 84 (2022).
date_created: 2022-06-17T16:16:15Z
date_published: 2022-06-17T00:00:00Z
date_updated: 2023-08-03T07:20:53Z
day: '17'
ddc:
- '510'
- '570'
department:
- _id: GradSch
- _id: NiBa
- _id: JaMa
doi: 10.1007/s11538-022-01029-z
ec_funded: 1
external_id:
isi:
- '000812509800001'
file:
- access_level: open_access
checksum: 05a1fe7d10914a00c2bca9b447993a65
content_type: application/pdf
creator: dernst
date_created: 2022-06-20T07:51:32Z
date_updated: 2022-06-20T07:51:32Z
file_id: '11455'
file_name: 2022_BulletinMathBiology_Saona.pdf
file_size: 463025
relation: main_file
success: 1
file_date_updated: 2022-06-20T07:51:32Z
has_accepted_license: '1'
intvolume: ' 84'
isi: 1
issue: '8'
keyword:
- Computational Theory and Mathematics
- General Agricultural and Biological Sciences
- Pharmacology
- General Environmental Science
- General Biochemistry
- Genetics and Molecular Biology
- General Mathematics
- Immunology
- General Neuroscience
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
project:
- _id: 26580278-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '771209'
name: Characterizing the fitness landscape on population and global scales
- _id: c098eddd-5a5b-11eb-8a69-abe27170a68f
grant_number: I05127
name: Evolutionary analysis of gene regulation
publication: Bulletin of Mathematical Biology
publication_identifier:
eissn:
- 1522-9602
issn:
- 0092-8240
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1007/s11538-022-01118-z
scopus_import: '1'
status: public
title: Relation between the number of peaks and the number of reciprocal sign epistatic
interactions
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 84
year: '2022'
...
---
_id: '11448'
abstract:
- lang: eng
text: Studies of protein fitness landscapes reveal biophysical constraints guiding
protein evolution and empower prediction of functional proteins. However, generalisation
of these findings is limited due to scarceness of systematic data on fitness landscapes
of proteins with a defined evolutionary relationship. We characterized the fitness
peaks of four orthologous fluorescent proteins with a broad range of sequence
divergence. While two of the four studied fitness peaks were sharp, the other
two were considerably flatter, being almost entirely free of epistatic interactions.
Mutationally robust proteins, characterized by a flat fitness peak, were not optimal
templates for machine-learning-driven protein design – instead, predictions were
more accurate for fragile proteins with epistatic landscapes. Our work paves insights
for practical application of fitness landscape heterogeneity in protein engineering.
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
acknowledgement: "We thank Ondřej Draganov, Rodrigo Redondo, Bor Kavčič, Mia Juračić
and Andrea Pauli for discussion and technical advice. We thank Anita Testa Salmazo
for advice on resin protein purification, Dmitry Bolotin and the Milaboratory (milaboratory.com)
for access to computing and storage infrastructure, and Josef Houser and Eva Fujdiarova
for technical assistance and data interpretation. Core facility Biomolecular Interactions
and Crystallization of CEITEC Masaryk University is gratefully acknowledged for
the obtaining of the scientific data presented in this paper. This research was
supported by the Scientific Service Units (SSU) of IST-Austria\r\nthrough resources
provided by the Bioimaging Facility (BIF), and the Life Science Facility (LSF).
MiSeq and HiSeq NGS sequencing was performed by the Next Generation Sequencing Facility
at Vienna BioCenter Core Facilities (VBCF), member of the Vienna BioCenter (VBC),
Austria. FACS was performed at the BioOptics Facility of the Institute of Molecular
Pathology (IMP), Austria. We also thank the Biomolecular Crystallography Facility
in the Vanderbilt University Center for Structural Biology. We are grateful to Joel
M Harp for help with X-ray data collection. This work was supported by the ERC Consolidator
grant to FAK (771209—CharFL). KSS acknowledges support by President’s Grant МК–5405.2021.1.4,
the Imperial College Research Fellowship and the MRC London Institute of Medical
Sciences (UKRI MC-A658-5QEA0).\r\nAF is supported by the Marie Skłodowska-Curie
Fellowship (H2020-MSCA-IF-2019, Grant Agreement No. 898203, Project acronym \"FLINDIP\").
Experiments were partially carried out using equipment provided by the Institute
of Bioorganic Chemistry of the Russian Academy of Sciences Сore Facility (CKP IBCH).
This work was supported by a Russian Science Foundation grant 19-74-10102.This project
has received funding from the European Union’s Horizon 2020 research and innovation
programme under the Marie Skłodowska-Curie Grant Agreement No. 665,385."
article_number: '75842'
article_processing_charge: No
article_type: original
author:
- first_name: Louisa
full_name: Gonzalez Somermeyer, Louisa
id: 4720D23C-F248-11E8-B48F-1D18A9856A87
last_name: Gonzalez Somermeyer
orcid: 0000-0001-9139-5383
- first_name: Aubin
full_name: Fleiss, Aubin
last_name: Fleiss
- first_name: Alexander S
full_name: Mishin, Alexander S
last_name: Mishin
- first_name: Nina G
full_name: Bozhanova, Nina G
last_name: Bozhanova
- first_name: Anna A
full_name: Igolkina, Anna A
last_name: Igolkina
- first_name: Jens
full_name: Meiler, Jens
last_name: Meiler
- first_name: Maria-Elisenda
full_name: Alaball Pujol, Maria-Elisenda
last_name: Alaball Pujol
- first_name: Ekaterina V
full_name: Putintseva, Ekaterina V
last_name: Putintseva
- first_name: Karen S
full_name: Sarkisyan, Karen S
last_name: Sarkisyan
- first_name: Fyodor
full_name: Kondrashov, Fyodor
id: 44FDEF62-F248-11E8-B48F-1D18A9856A87
last_name: Kondrashov
orcid: 0000-0001-8243-4694
citation:
ama: Gonzalez Somermeyer L, Fleiss A, Mishin AS, et al. Heterogeneity of the GFP
fitness landscape and data-driven protein design. eLife. 2022;11. doi:10.7554/elife.75842
apa: Gonzalez Somermeyer, L., Fleiss, A., Mishin, A. S., Bozhanova, N. G., Igolkina,
A. A., Meiler, J., … Kondrashov, F. (2022). Heterogeneity of the GFP fitness landscape
and data-driven protein design. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.75842
chicago: Gonzalez Somermeyer, Louisa, Aubin Fleiss, Alexander S Mishin, Nina G Bozhanova,
Anna A Igolkina, Jens Meiler, Maria-Elisenda Alaball Pujol, Ekaterina V Putintseva,
Karen S Sarkisyan, and Fyodor Kondrashov. “Heterogeneity of the GFP Fitness Landscape
and Data-Driven Protein Design.” ELife. eLife Sciences Publications, 2022.
https://doi.org/10.7554/elife.75842.
ieee: L. Gonzalez Somermeyer et al., “Heterogeneity of the GFP fitness landscape
and data-driven protein design,” eLife, vol. 11. eLife Sciences Publications,
2022.
ista: Gonzalez Somermeyer L, Fleiss A, Mishin AS, Bozhanova NG, Igolkina AA, Meiler
J, Alaball Pujol M-E, Putintseva EV, Sarkisyan KS, Kondrashov F. 2022. Heterogeneity
of the GFP fitness landscape and data-driven protein design. eLife. 11, 75842.
mla: Gonzalez Somermeyer, Louisa, et al. “Heterogeneity of the GFP Fitness Landscape
and Data-Driven Protein Design.” ELife, vol. 11, 75842, eLife Sciences
Publications, 2022, doi:10.7554/elife.75842.
short: L. Gonzalez Somermeyer, A. Fleiss, A.S. Mishin, N.G. Bozhanova, A.A. Igolkina,
J. Meiler, M.-E. Alaball Pujol, E.V. Putintseva, K.S. Sarkisyan, F. Kondrashov,
ELife 11 (2022).
date_created: 2022-06-18T09:06:59Z
date_published: 2022-05-05T00:00:00Z
date_updated: 2023-08-03T07:20:15Z
day: '05'
ddc:
- '570'
department:
- _id: GradSch
- _id: FyKo
doi: 10.7554/elife.75842
ec_funded: 1
external_id:
isi:
- '000799197200001'
file:
- access_level: open_access
checksum: 7573c28f44028ab0cc81faef30039e44
content_type: application/pdf
creator: dernst
date_created: 2022-06-20T07:44:19Z
date_updated: 2022-06-20T07:44:19Z
file_id: '11454'
file_name: 2022_eLife_Somermeyer.pdf
file_size: 5297213
relation: main_file
success: 1
file_date_updated: 2022-06-20T07:44:19Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 26580278-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '771209'
name: Characterizing the fitness landscape on population and global scales
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Heterogeneity of the GFP fitness landscape and data-driven protein design
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2022'
...
---
_id: '10639'
abstract:
- lang: eng
text: With more than 80 members worldwide, the Orthobunyavirus genus in the Peribunyaviridae
family is a large genus of enveloped RNA viruses, many of which are emerging pathogens
in humans and livestock. How orthobunyaviruses (OBVs) penetrate and infect mammalian
host cells remains poorly characterized. Here, we investigated the entry mechanisms
of the OBV Germiston (GERV). Viral particles were visualized by cryo-electron
microscopy and appeared roughly spherical with an average diameter of 98 nm. Labeling
of the virus with fluorescent dyes did not adversely affect its infectivity and
allowed the monitoring of single particles in fixed and live cells. Using this
approach, we found that endocytic internalization of bound viruses was asynchronous
and occurred within 30-40 min. The virus entered Rab5a+ early endosomes and, subsequently,
late endosomal vacuoles containing Rab7a but not LAMP-1. Infectious entry did
not require proteolytic cleavage, and endosomal acidification was sufficient and
necessary for viral fusion. Acid-activated penetration began 15-25 min after initiation
of virus internalization and relied on maturation of early endosomes to late endosomes.
The optimal pH for viral membrane fusion was slightly below 6.0, and penetration
was hampered when the potassium influx was abolished. Overall, our study provides
real-time visualization of GERV entry into host cells and demonstrates the importance
of late endosomal maturation in facilitating OBV penetration.
acknowledged_ssus:
- _id: EM-Fac
acknowledgement: This work was supported by INRAE starter funds, Project IDEXLYON (University of Lyon)
within the Programme Investissements d’Avenir (ANR-16-IDEX-0005), and FINOVIAO14
(Fondation pour l’Université de Lyon), all to P.Y.L. This work was also supported by
CellNetworks Research Group funds and Deutsche Forschungsgemeinschaft (DFG) funding
(grant numbers LO-2338/1-1 and LO-2338/3-1) awarded to P.Y.L., Austrian Science Fund
(FWF) grant P31445 to F.K.M.S., a Chinese Scholarship Council (CSC;no. 201904910701)
fellowship to Q.X., and a ministére de l’enseignement supérieur, de la recherche et de
l’innovation (MESRI) doctoral thesis grant to M.D.
article_number: e02146-21
article_processing_charge: No
article_type: original
author:
- first_name: Stefan
full_name: Windhaber, Stefan
last_name: Windhaber
- first_name: Qilin
full_name: Xin, Qilin
last_name: Xin
- first_name: Zina M.
full_name: Uckeley, Zina M.
last_name: Uckeley
- first_name: Jana
full_name: Koch, Jana
last_name: Koch
- first_name: Martin
full_name: Obr, Martin
id: 4741CA5A-F248-11E8-B48F-1D18A9856A87
last_name: Obr
- first_name: Céline
full_name: Garnier, Céline
last_name: Garnier
- first_name: Catherine
full_name: Luengo-Guyonnot, Catherine
last_name: Luengo-Guyonnot
- first_name: Maëva
full_name: Duboeuf, Maëva
last_name: Duboeuf
- first_name: Florian KM
full_name: Schur, Florian KM
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
- first_name: Pierre-Yves
full_name: Lozach, Pierre-Yves
last_name: Lozach
citation:
ama: Windhaber S, Xin Q, Uckeley ZM, et al. The Orthobunyavirus Germiston enters
host cells from late endosomes. Journal of Virology. 2022;96(5). doi:10.1128/jvi.02146-21
apa: Windhaber, S., Xin, Q., Uckeley, Z. M., Koch, J., Obr, M., Garnier, C., … Lozach,
P.-Y. (2022). The Orthobunyavirus Germiston enters host cells from late endosomes.
Journal of Virology. American Society for Microbiology. https://doi.org/10.1128/jvi.02146-21
chicago: Windhaber, Stefan, Qilin Xin, Zina M. Uckeley, Jana Koch, Martin Obr, Céline
Garnier, Catherine Luengo-Guyonnot, Maëva Duboeuf, Florian KM Schur, and Pierre-Yves
Lozach. “The Orthobunyavirus Germiston Enters Host Cells from Late Endosomes.”
Journal of Virology. American Society for Microbiology, 2022. https://doi.org/10.1128/jvi.02146-21.
ieee: S. Windhaber et al., “The Orthobunyavirus Germiston enters host cells
from late endosomes,” Journal of Virology, vol. 96, no. 5. American Society
for Microbiology, 2022.
ista: Windhaber S, Xin Q, Uckeley ZM, Koch J, Obr M, Garnier C, Luengo-Guyonnot
C, Duboeuf M, Schur FK, Lozach P-Y. 2022. The Orthobunyavirus Germiston enters
host cells from late endosomes. Journal of Virology. 96(5), e02146-21.
mla: Windhaber, Stefan, et al. “The Orthobunyavirus Germiston Enters Host Cells
from Late Endosomes.” Journal of Virology, vol. 96, no. 5, e02146-21, American
Society for Microbiology, 2022, doi:10.1128/jvi.02146-21.
short: S. Windhaber, Q. Xin, Z.M. Uckeley, J. Koch, M. Obr, C. Garnier, C. Luengo-Guyonnot,
M. Duboeuf, F.K. Schur, P.-Y. Lozach, Journal of Virology 96 (2022).
date_created: 2022-01-18T10:04:18Z
date_published: 2022-03-01T00:00:00Z
date_updated: 2023-08-02T13:52:33Z
day: '01'
department:
- _id: FlSc
doi: 10.1128/jvi.02146-21
external_id:
isi:
- '000779305000033'
pmid:
- '35019710'
intvolume: ' 96'
isi: 1
issue: '5'
keyword:
- virology
- insect science
- immunology
- microbiology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8906410
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 26736D6A-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P31445
name: Structural conservation and diversity in retroviral capsid
publication: Journal of Virology
publication_identifier:
eissn:
- 1098-5514
issn:
- 0022-538X
publication_status: published
publisher: American Society for Microbiology
quality_controlled: '1'
scopus_import: '1'
status: public
title: The Orthobunyavirus Germiston enters host cells from late endosomes
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 96
year: '2022'
...
---
_id: '12117'
abstract:
- lang: eng
text: "To understand how potential gene manipulations affect in vitro microglia,
we provide a set of short protocols to evaluate microglia identity and function.
We detail steps for immunostaining to determine microglia identity. We describe
three functional assays for microglia: phagocytosis, calcium response following
ATP stimulation, and cytokine expression upon inflammatory stimuli. We apply these
protocols to human induced-pluripotent-stem-cell (hiPSC)-derived microglia, but
they can be also applied to other in vitro microglial models including primary
mouse microglia.\r\nFor complete details on the use and execution of this protocol,
please refer to Bartalska et al. (2022).1"
acknowledged_ssus:
- _id: Bio
acknowledgement: This project has received funding from the European Research Council
(ERC) under the European Union’s Horizon 2020 research and innovation program (grant
No. 715571 to S.S.) and from the Gesellschaft für Forschungsförderung Niederösterreich
(grant No. Sc19-017 to V.H.). We thank Rouven Schulz and Alessandro Venturino for
their insights into functional assays and data analysis, Verena Seiboth for insights
into necessary institutional permission, and ISTA imaging & optics facility (IOF)
especially Bernhard Hochreiter for their support.
article_number: '101866'
article_processing_charge: No
article_type: letter_note
author:
- first_name: Verena
full_name: Hübschmann, Verena
id: 32B7C918-F248-11E8-B48F-1D18A9856A87
last_name: Hübschmann
- first_name: Medina
full_name: Korkut, Medina
id: 4B51CE74-F248-11E8-B48F-1D18A9856A87
last_name: Korkut
orcid: 0000-0003-4309-2251
- first_name: Sandra
full_name: Siegert, Sandra
id: 36ACD32E-F248-11E8-B48F-1D18A9856A87
last_name: Siegert
orcid: 0000-0001-8635-0877
citation:
ama: Hübschmann V, Korkut M, Siegert S. Assessing human iPSC-derived microglia identity
and function by immunostaining, phagocytosis, calcium activity, and inflammation
assay. STAR Protocols. 2022;3(4). doi:10.1016/j.xpro.2022.101866
apa: Hübschmann, V., Korkut, M., & Siegert, S. (2022). Assessing human iPSC-derived
microglia identity and function by immunostaining, phagocytosis, calcium activity,
and inflammation assay. STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2022.101866
chicago: Hübschmann, Verena, Medina Korkut, and Sandra Siegert. “Assessing Human
IPSC-Derived Microglia Identity and Function by Immunostaining, Phagocytosis,
Calcium Activity, and Inflammation Assay.” STAR Protocols. Elsevier, 2022.
https://doi.org/10.1016/j.xpro.2022.101866.
ieee: V. Hübschmann, M. Korkut, and S. Siegert, “Assessing human iPSC-derived microglia
identity and function by immunostaining, phagocytosis, calcium activity, and inflammation
assay,” STAR Protocols, vol. 3, no. 4. Elsevier, 2022.
ista: Hübschmann V, Korkut M, Siegert S. 2022. Assessing human iPSC-derived microglia
identity and function by immunostaining, phagocytosis, calcium activity, and inflammation
assay. STAR Protocols. 3(4), 101866.
mla: Hübschmann, Verena, et al. “Assessing Human IPSC-Derived Microglia Identity
and Function by Immunostaining, Phagocytosis, Calcium Activity, and Inflammation
Assay.” STAR Protocols, vol. 3, no. 4, 101866, Elsevier, 2022, doi:10.1016/j.xpro.2022.101866.
short: V. Hübschmann, M. Korkut, S. Siegert, STAR Protocols 3 (2022).
date_created: 2023-01-12T11:56:38Z
date_published: 2022-12-16T00:00:00Z
date_updated: 2023-11-02T12:21:32Z
day: '16'
ddc:
- '570'
department:
- _id: SaSi
- _id: GradSch
doi: 10.1016/j.xpro.2022.101866
ec_funded: 1
file:
- access_level: open_access
checksum: 3c71b8a60633d42c2f77c49025d5559b
content_type: application/pdf
creator: dernst
date_created: 2023-01-23T09:50:51Z
date_updated: 2023-01-23T09:50:51Z
file_id: '12340'
file_name: 2022_STARProtocols_Huebschmann.pdf
file_size: 6251945
relation: main_file
success: 1
file_date_updated: 2023-01-23T09:50:51Z
has_accepted_license: '1'
intvolume: ' 3'
issue: '4'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Neuroscience
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 25D4A630-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '715571'
name: Microglia action towards neuronal circuit formation and function in health
and disease
- _id: 9B99D380-BA93-11EA-9121-9846C619BF3A
grant_number: SC19-017
name: How human microglia shape developing neurons during health and inflammation
publication: STAR Protocols
publication_identifier:
issn:
- 2666-1667
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
record:
- id: '11478'
relation: other
status: public
scopus_import: '1'
status: public
title: Assessing human iPSC-derived microglia identity and function by immunostaining,
phagocytosis, calcium activity, and inflammation assay
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 3
year: '2022'
...
---
_id: '12119'
abstract:
- lang: eng
text: Intravascular neutrophils and platelets collaborate in maintaining host integrity,
but their interaction can also trigger thrombotic complications. We report here
that cooperation between neutrophil and platelet lineages extends to the earliest
stages of platelet formation by megakaryocytes in the bone marrow. Using intravital
microscopy, we show that neutrophils “plucked” intravascular megakaryocyte extensions,
termed proplatelets, to control platelet production. Following CXCR4-CXCL12-dependent
migration towards perisinusoidal megakaryocytes, plucking neutrophils actively
pulled on proplatelets and triggered myosin light chain and extracellular-signal-regulated
kinase activation through reactive oxygen species. By these mechanisms, neutrophils
accelerate proplatelet growth and facilitate continuous release of platelets in
steady state. Following myocardial infarction, plucking neutrophils drove excessive
release of young, reticulated platelets and boosted the risk of recurrent ischemia.
Ablation of neutrophil plucking normalized thrombopoiesis and reduced recurrent
thrombosis after myocardial infarction and thrombus burden in venous thrombosis.
We establish neutrophil plucking as a target to reduce thromboischemic events.
acknowledgement: "We thank Coung Kieu and Dominik van den Heuvel for excellent technical
assistance. This work was supported by the German Research Foundation (PE2704/2-1,
PE2704/3-1 to T.P., SFB 1123-project B06 to S.M., SFB1525 project A07 to D.S, TRR
332 project A7 to C.S., PO 2247/2-1 to A.P., SFB1116-project B11 to A.P. and B12
to M.K.), LMU Munich’s Institutional\r\nStrategy LMUexcellent within the framework
of the German Excellence Initiative (No. 806 32 006 to T.P.), and by the German
Centre for Cardiovascular Research (DZHK) to T.P. (Postdoc Start-up grant No. 100378833).
This project has received funding from the European Research Council (ERC) under
the European Union’s Horizon 2020 research and innovation program (grant agreement
No. 833440 to S.M.). F.G. received funding from the European Union’s\r\nHorizon
2020 research and innovation program under the Marie Sk1odowska-Curie grant agreement
no. 747687. A.H. was funded by RTI2018-095497-B-I00 from Ministerio de Ciencia e
Innovacio´ n (MICINN), HR17_00527 from Fundacion La Caixa, and Transatlantic Network
of Excellence (TNE-18CVD04) from the Leducq Foundation. The CNIC is supported by
the MICINN and the Pro CNIC Foundation and is a Severo Ochoa Center of Excellence
(CEX2020-001041-S). A.P. was supported by the Forschungskommission of the Medical
Faculty of the Heinrich-Heine-Universität Düsseldorf (No. 18-2019 to A.P.). C.G.
was supported by the Helmholtz Alliance ‘Aging and Metabolic Programming, AMPro,’
by the German Federal\r\nMinistry of Education and Research to the German Center
for Diabetes Research (DZD), and by the Bavarian State Ministry of Health and Care
through the research project DigiMed Bayern."
article_processing_charge: No
article_type: original
author:
- first_name: Tobias
full_name: Petzold, Tobias
last_name: Petzold
- first_name: Zhe
full_name: Zhang, Zhe
last_name: Zhang
- first_name: Iván
full_name: Ballesteros, Iván
last_name: Ballesteros
- first_name: Inas
full_name: Saleh, Inas
last_name: Saleh
- first_name: Amin
full_name: Polzin, Amin
last_name: Polzin
- first_name: Manuela
full_name: Thienel, Manuela
last_name: Thienel
- first_name: Lulu
full_name: Liu, Lulu
last_name: Liu
- first_name: Qurrat
full_name: Ul Ain, Qurrat
last_name: Ul Ain
- first_name: Vincent
full_name: Ehreiser, Vincent
last_name: Ehreiser
- first_name: Christian
full_name: Weber, Christian
last_name: Weber
- first_name: Badr
full_name: Kilani, Badr
last_name: Kilani
- first_name: Pontus
full_name: Mertsch, Pontus
last_name: Mertsch
- first_name: Jeremias
full_name: Götschke, Jeremias
last_name: Götschke
- first_name: Sophie
full_name: Cremer, Sophie
last_name: Cremer
- first_name: Wenwen
full_name: Fu, Wenwen
last_name: Fu
- first_name: Michael
full_name: Lorenz, Michael
last_name: Lorenz
- first_name: Hellen
full_name: Ishikawa-Ankerhold, Hellen
last_name: Ishikawa-Ankerhold
- first_name: Elisabeth
full_name: Raatz, Elisabeth
last_name: Raatz
- first_name: Shaza
full_name: El-Nemr, Shaza
last_name: El-Nemr
- first_name: Agnes
full_name: Görlach, Agnes
last_name: Görlach
- first_name: Esther
full_name: Marhuenda, Esther
last_name: Marhuenda
- first_name: Konstantin
full_name: Stark, Konstantin
last_name: Stark
- first_name: Joachim
full_name: Pircher, Joachim
last_name: Pircher
- first_name: David
full_name: Stegner, David
last_name: Stegner
- first_name: Christian
full_name: Gieger, Christian
last_name: Gieger
- first_name: Marc
full_name: Schmidt-Supprian, Marc
last_name: Schmidt-Supprian
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Isaac
full_name: Almendros, Isaac
last_name: Almendros
- first_name: Malte
full_name: Kelm, Malte
last_name: Kelm
- first_name: Christian
full_name: Schulz, Christian
last_name: Schulz
- first_name: Andrés
full_name: Hidalgo, Andrés
last_name: Hidalgo
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
citation:
ama: Petzold T, Zhang Z, Ballesteros I, et al. Neutrophil “plucking” on megakaryocytes
drives platelet production and boosts cardiovascular disease. Immunity.
2022;55(12):2285-2299.e7. doi:10.1016/j.immuni.2022.10.001
apa: Petzold, T., Zhang, Z., Ballesteros, I., Saleh, I., Polzin, A., Thienel, M.,
… Massberg, S. (2022). Neutrophil “plucking” on megakaryocytes drives platelet
production and boosts cardiovascular disease. Immunity. Elsevier. https://doi.org/10.1016/j.immuni.2022.10.001
chicago: Petzold, Tobias, Zhe Zhang, Iván Ballesteros, Inas Saleh, Amin Polzin,
Manuela Thienel, Lulu Liu, et al. “Neutrophil ‘Plucking’ on Megakaryocytes Drives
Platelet Production and Boosts Cardiovascular Disease.” Immunity. Elsevier,
2022. https://doi.org/10.1016/j.immuni.2022.10.001.
ieee: T. Petzold et al., “Neutrophil ‘plucking’ on megakaryocytes drives
platelet production and boosts cardiovascular disease,” Immunity, vol.
55, no. 12. Elsevier, p. 2285–2299.e7, 2022.
ista: Petzold T, Zhang Z, Ballesteros I, Saleh I, Polzin A, Thienel M, Liu L, Ul
Ain Q, Ehreiser V, Weber C, Kilani B, Mertsch P, Götschke J, Cremer S, Fu W, Lorenz
M, Ishikawa-Ankerhold H, Raatz E, El-Nemr S, Görlach A, Marhuenda E, Stark K,
Pircher J, Stegner D, Gieger C, Schmidt-Supprian M, Gärtner FR, Almendros I, Kelm
M, Schulz C, Hidalgo A, Massberg S. 2022. Neutrophil “plucking” on megakaryocytes
drives platelet production and boosts cardiovascular disease. Immunity. 55(12),
2285–2299.e7.
mla: Petzold, Tobias, et al. “Neutrophil ‘Plucking’ on Megakaryocytes Drives Platelet
Production and Boosts Cardiovascular Disease.” Immunity, vol. 55, no. 12,
Elsevier, 2022, p. 2285–2299.e7, doi:10.1016/j.immuni.2022.10.001.
short: T. Petzold, Z. Zhang, I. Ballesteros, I. Saleh, A. Polzin, M. Thienel, L.
Liu, Q. Ul Ain, V. Ehreiser, C. Weber, B. Kilani, P. Mertsch, J. Götschke, S.
Cremer, W. Fu, M. Lorenz, H. Ishikawa-Ankerhold, E. Raatz, S. El-Nemr, A. Görlach,
E. Marhuenda, K. Stark, J. Pircher, D. Stegner, C. Gieger, M. Schmidt-Supprian,
F.R. Gärtner, I. Almendros, M. Kelm, C. Schulz, A. Hidalgo, S. Massberg, Immunity
55 (2022) 2285–2299.e7.
date_created: 2023-01-12T11:56:54Z
date_published: 2022-12-13T00:00:00Z
date_updated: 2023-08-03T14:21:51Z
day: '13'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.immuni.2022.10.001
ec_funded: 1
external_id:
isi:
- '000922019600003'
pmid:
- '36272416'
file:
- access_level: open_access
checksum: 073267a9c0ad9f85a650053bc7b23777
content_type: application/pdf
creator: dernst
date_created: 2023-01-23T10:18:48Z
date_updated: 2023-01-23T10:18:48Z
file_id: '12341'
file_name: 2022_Immunity_Petzold.pdf
file_size: 5299475
relation: main_file
success: 1
file_date_updated: 2023-01-23T10:18:48Z
has_accepted_license: '1'
intvolume: ' 55'
isi: 1
issue: '12'
keyword:
- Infectious Diseases
- Immunology
- Immunology and Allergy
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 2285-2299.e7
pmid: 1
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Immunity
publication_identifier:
issn:
- 1074-7613
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Neutrophil “plucking” on megakaryocytes drives platelet production and boosts
cardiovascular disease
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 55
year: '2022'
...
---
_id: '12131'
abstract:
- lang: eng
text: Replication-incompetent adenoviral vectors have been extensively used as a
platform for vaccine design, with at least four anti-COVID-19 vaccines authorized
to date. These vaccines elicit neutralizing antibody responses directed against
SARS-CoV-2 Spike protein and confer significant level of protection against SARS-CoV-2
infection. Immunization with adenovirus-vectored vaccines is known to be accompanied
by the production of anti-vector antibodies, which may translate into reduced
efficacy of booster or repeated rounds of revaccination. Here, we used blood samples
from patients who received an adenovirus-based Gam-COVID-Vac vaccine to address
the question of whether anti-vector antibodies may influence the magnitude of
SARS-CoV-2-specific humoral response after booster vaccination. We observed that
rAd26-based prime vaccination with Gam-COVID-Vac induced the development of Ad26-neutralizing
antibodies, which persisted in circulation for at least 9 months. Our analysis
further indicates that high pre-boost Ad26 neutralizing antibody titers do not
appear to affect the humoral immunogenicity of the Gam-COVID-Vac boost. The titers
of anti-SARS-CoV-2 RBD IgGs and antibodies, which neutralized both the wild type
and the circulating variants of concern of SARS-CoV-2 such as Delta and Omicron,
were independent of the pre-boost levels of Ad26-neutralizing antibodies. Thus,
our results support the development of repeated immunization schedule with adenovirus-based
COVID-19 vaccines.
acknowledgement: We thank Sergey Kulemzin, Grigory Efimov, Yuri Lebedin, Alexander
Taranin and Rudolf Valenta for providing reagents. Figures were created with the
help of BioRender.com. This work was supported by the Russian Science Foundation
(Project 21-15-00286). Byazrova M.G. was supported by the RUDN University Strategic
Academic Leadership Program.
article_number: '145'
article_processing_charge: No
article_type: original
author:
- first_name: Maria G.
full_name: Byazrova, Maria G.
last_name: Byazrova
- first_name: Ekaterina A.
full_name: Astakhova, Ekaterina A.
last_name: Astakhova
- first_name: Aygul
full_name: Minnegalieva, Aygul
id: 87DF77F0-1D9A-11EA-B6AE-CE443DDC885E
last_name: Minnegalieva
- first_name: Maria M.
full_name: Sukhova, Maria M.
last_name: Sukhova
- first_name: Artem A.
full_name: Mikhailov, Artem A.
last_name: Mikhailov
- first_name: Alexey G.
full_name: Prilipov, Alexey G.
last_name: Prilipov
- first_name: Andrey A.
full_name: Gorchakov, Andrey A.
last_name: Gorchakov
- first_name: Alexander V.
full_name: Filatov, Alexander V.
last_name: Filatov
citation:
ama: Byazrova MG, Astakhova EA, Minnegalieva A, et al. Anti-Ad26 humoral immunity
does not compromise SARS-COV-2 neutralizing antibody responses following Gam-COVID-Vac
booster vaccination. npj Vaccines. 2022;7. doi:10.1038/s41541-022-00566-x
apa: Byazrova, M. G., Astakhova, E. A., Minnegalieva, A., Sukhova, M. M., Mikhailov,
A. A., Prilipov, A. G., … Filatov, A. V. (2022). Anti-Ad26 humoral immunity does
not compromise SARS-COV-2 neutralizing antibody responses following Gam-COVID-Vac
booster vaccination. Npj Vaccines. Springer Nature. https://doi.org/10.1038/s41541-022-00566-x
chicago: Byazrova, Maria G., Ekaterina A. Astakhova, Aygul Minnegalieva, Maria M.
Sukhova, Artem A. Mikhailov, Alexey G. Prilipov, Andrey A. Gorchakov, and Alexander
V. Filatov. “Anti-Ad26 Humoral Immunity Does Not Compromise SARS-COV-2 Neutralizing
Antibody Responses Following Gam-COVID-Vac Booster Vaccination.” Npj Vaccines.
Springer Nature, 2022. https://doi.org/10.1038/s41541-022-00566-x.
ieee: M. G. Byazrova et al., “Anti-Ad26 humoral immunity does not compromise
SARS-COV-2 neutralizing antibody responses following Gam-COVID-Vac booster vaccination,”
npj Vaccines, vol. 7. Springer Nature, 2022.
ista: Byazrova MG, Astakhova EA, Minnegalieva A, Sukhova MM, Mikhailov AA, Prilipov
AG, Gorchakov AA, Filatov AV. 2022. Anti-Ad26 humoral immunity does not compromise
SARS-COV-2 neutralizing antibody responses following Gam-COVID-Vac booster vaccination.
npj Vaccines. 7, 145.
mla: Byazrova, Maria G., et al. “Anti-Ad26 Humoral Immunity Does Not Compromise
SARS-COV-2 Neutralizing Antibody Responses Following Gam-COVID-Vac Booster Vaccination.”
Npj Vaccines, vol. 7, 145, Springer Nature, 2022, doi:10.1038/s41541-022-00566-x.
short: M.G. Byazrova, E.A. Astakhova, A. Minnegalieva, M.M. Sukhova, A.A. Mikhailov,
A.G. Prilipov, A.A. Gorchakov, A.V. Filatov, Npj Vaccines 7 (2022).
date_created: 2023-01-12T12:02:54Z
date_published: 2022-11-15T00:00:00Z
date_updated: 2023-08-04T08:52:40Z
day: '15'
ddc:
- '570'
department:
- _id: FyKo
doi: 10.1038/s41541-022-00566-x
external_id:
isi:
- '000884278600004'
pmid:
- '36379998'
file:
- access_level: open_access
checksum: ddaac096381565b2b4b7dcc34cdbc4ee
content_type: application/pdf
creator: dernst
date_created: 2023-01-23T11:22:09Z
date_updated: 2023-01-23T11:22:09Z
file_id: '12347'
file_name: 2022_njpVaccines_Byazrova.pdf
file_size: 1856046
relation: main_file
success: 1
file_date_updated: 2023-01-23T11:22:09Z
has_accepted_license: '1'
intvolume: ' 7'
isi: 1
keyword:
- Pharmacology (medical)
- Infectious Diseases
- Pharmacology
- Immunology
- SARS-COV-2
- COVID
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: npj Vaccines
publication_identifier:
issn:
- 2059-0105
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Anti-Ad26 humoral immunity does not compromise SARS-COV-2 neutralizing antibody
responses following Gam-COVID-Vac booster vaccination
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 7
year: '2022'
...
---
_id: '12157'
abstract:
- lang: eng
text: 'Polygenic adaptation is thought to be ubiquitous, yet remains poorly understood.
Here, we model this process analytically, in the plausible setting of a highly
polygenic, quantitative trait that experiences a sudden shift in the fitness optimum.
We show how the mean phenotype changes over time, depending on the effect sizes
of loci that contribute to variance in the trait, and characterize the allele
dynamics at these loci. Notably, we describe the two phases of the allele dynamics:
The first is a rapid phase, in which directional selection introduces small frequency
differences between alleles whose effects are aligned with or opposed to the shift,
ultimately leading to small differences in their probability of fixation during
a second, longer phase, governed by stabilizing selection. As we discuss, key
results should hold in more general settings and have important implications for
efforts to identify the genetic basis of adaptation in humans and other species.'
acknowledgement: "We thank Guy Amster, Jeremy Berg, Nick Barton, Yuval Simons and
Molly Przeworski for many helpful discussions, and Jeremy Berg, Graham Coop, Joachim
Hermisson, Guillaume Martin, Will Milligan, Peter Ralph, Yuval Simons, Leo Speidel
and Molly Przeworski for comments on the manuscript.\r\nNational Institutes of Health
GM115889 Laura Katharine Hayward Guy Sella \r\nNational Institutes of Health GM121372
Laura Katharine Hayward"
article_number: '66697'
article_processing_charge: No
article_type: original
author:
- first_name: Laura
full_name: Hayward, Laura
id: fc885ee5-24bf-11eb-ad7b-bcc5104c0c1b
last_name: Hayward
- first_name: Guy
full_name: Sella, Guy
last_name: Sella
citation:
ama: Hayward L, Sella G. Polygenic adaptation after a sudden change in environment.
eLife. 2022;11. doi:10.7554/elife.66697
apa: Hayward, L., & Sella, G. (2022). Polygenic adaptation after a sudden change
in environment. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.66697
chicago: Hayward, Laura, and Guy Sella. “Polygenic Adaptation after a Sudden Change
in Environment.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/elife.66697.
ieee: L. Hayward and G. Sella, “Polygenic adaptation after a sudden change in environment,”
eLife, vol. 11. eLife Sciences Publications, 2022.
ista: Hayward L, Sella G. 2022. Polygenic adaptation after a sudden change in environment.
eLife. 11, 66697.
mla: Hayward, Laura, and Guy Sella. “Polygenic Adaptation after a Sudden Change
in Environment.” ELife, vol. 11, 66697, eLife Sciences Publications, 2022,
doi:10.7554/elife.66697.
short: L. Hayward, G. Sella, ELife 11 (2022).
date_created: 2023-01-12T12:09:00Z
date_published: 2022-09-26T00:00:00Z
date_updated: 2023-08-04T09:04:58Z
day: '26'
ddc:
- '570'
department:
- _id: NiBa
doi: 10.7554/elife.66697
external_id:
isi:
- '000890735600001'
file:
- access_level: open_access
checksum: 28de155b231ac1c8d4501c98b2fb359a
content_type: application/pdf
creator: dernst
date_created: 2023-01-24T12:21:32Z
date_updated: 2023-01-24T12:21:32Z
file_id: '12363'
file_name: 2022_eLife_Hayward.pdf
file_size: 18935612
relation: main_file
success: 1
file_date_updated: 2023-01-24T12:21:32Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Polygenic adaptation after a sudden change in environment
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2022'
...
---
_id: '12252'
abstract:
- lang: eng
text: The COVID−19 pandemic not only resulted in a global crisis, but also accelerated
vaccine development and antibody discovery. Herein we report a synthetic humanized
VHH library development pipeline for nanomolar-range affinity VHH binders to SARS-CoV-2
variants of concern (VoC) receptor binding domains (RBD) isolation. Trinucleotide-based
randomization of CDRs by Kunkel mutagenesis with the subsequent rolling-cycle
amplification resulted in more than 1011 diverse phage display
library in a manageable for a single person number of electroporation reactions.
We identified a number of nanomolar-range affinity VHH binders to SARS-CoV-2 variants
of concern (VoC) receptor binding domains (RBD) by screening a novel synthetic
humanized antibody library. In order to explore the most robust and fast method
for affinity improvement, we performed affinity maturation by CDR1 and CDR2 shuffling
and avidity engineering by multivalent trimeric VHH fusion protein construction.
As a result, H7-Fc and G12x3-Fc binders were developed with the affinities in
nM and pM range respectively. Importantly, these affinities are weakly influenced
by most of SARS-CoV-2 VoC mutations and they retain moderate binding to BA.4\5.
The plaque reduction neutralization test (PRNT) resulted in IC50 = 100 ng\ml and
9.6 ng\ml for H7-Fc and G12x3-Fc antibodies, respectively, for the emerging Omicron
BA.1 variant. Therefore, these VHH could expand the present landscape of SARS-CoV-2
neutralization binders with the therapeutic potential for present and future SARS-CoV-2
variants.
acknowledgement: The authors declare that this study received funding from Immunofusion.
The funder was not involved in the study design, collection, analysis, interpretation
of data, the writing of this article or the decision to submit it for publication.
article_number: '965446'
article_processing_charge: No
article_type: original
author:
- first_name: Dmitri
full_name: Dormeshkin, Dmitri
last_name: Dormeshkin
- first_name: Michail
full_name: Shapira, Michail
last_name: Shapira
- first_name: Simon
full_name: Dubovik, Simon
last_name: Dubovik
- first_name: Anton
full_name: Kavaleuski, Anton
id: 4968f7ad-eb97-11eb-a6c2-8ed382e8912c
last_name: Kavaleuski
orcid: 0000-0003-2091-526X
- first_name: Mikalai
full_name: Katsin, Mikalai
last_name: Katsin
- first_name: Alexandr
full_name: Migas, Alexandr
last_name: Migas
- first_name: Alexander
full_name: Meleshko, Alexander
last_name: Meleshko
- first_name: Sergei
full_name: Semyonov, Sergei
last_name: Semyonov
citation:
ama: Dormeshkin D, Shapira M, Dubovik S, et al. Isolation of an escape-resistant
SARS-CoV-2 neutralizing nanobody from a novel synthetic nanobody library. Frontiers
in Immunology. 2022;13. doi:10.3389/fimmu.2022.965446
apa: Dormeshkin, D., Shapira, M., Dubovik, S., Kavaleuski, A., Katsin, M., Migas,
A., … Semyonov, S. (2022). Isolation of an escape-resistant SARS-CoV-2 neutralizing
nanobody from a novel synthetic nanobody library. Frontiers in Immunology.
Frontiers Media. https://doi.org/10.3389/fimmu.2022.965446
chicago: Dormeshkin, Dmitri, Michail Shapira, Simon Dubovik, Anton Kavaleuski, Mikalai
Katsin, Alexandr Migas, Alexander Meleshko, and Sergei Semyonov. “Isolation of
an Escape-Resistant SARS-CoV-2 Neutralizing Nanobody from a Novel Synthetic Nanobody
Library.” Frontiers in Immunology. Frontiers Media, 2022. https://doi.org/10.3389/fimmu.2022.965446.
ieee: D. Dormeshkin et al., “Isolation of an escape-resistant SARS-CoV-2
neutralizing nanobody from a novel synthetic nanobody library,” Frontiers in
Immunology, vol. 13. Frontiers Media, 2022.
ista: Dormeshkin D, Shapira M, Dubovik S, Kavaleuski A, Katsin M, Migas A, Meleshko
A, Semyonov S. 2022. Isolation of an escape-resistant SARS-CoV-2 neutralizing
nanobody from a novel synthetic nanobody library. Frontiers in Immunology. 13,
965446.
mla: Dormeshkin, Dmitri, et al. “Isolation of an Escape-Resistant SARS-CoV-2 Neutralizing
Nanobody from a Novel Synthetic Nanobody Library.” Frontiers in Immunology,
vol. 13, 965446, Frontiers Media, 2022, doi:10.3389/fimmu.2022.965446.
short: D. Dormeshkin, M. Shapira, S. Dubovik, A. Kavaleuski, M. Katsin, A. Migas,
A. Meleshko, S. Semyonov, Frontiers in Immunology 13 (2022).
date_created: 2023-01-16T09:56:57Z
date_published: 2022-09-16T00:00:00Z
date_updated: 2023-08-04T09:49:24Z
day: '16'
ddc:
- '570'
department:
- _id: LeSa
doi: 10.3389/fimmu.2022.965446
external_id:
isi:
- '000862479100001'
file:
- access_level: open_access
checksum: f8f5d8110710033d0532e7e08bf9dad4
content_type: application/pdf
creator: dernst
date_created: 2023-01-30T09:22:26Z
date_updated: 2023-01-30T09:22:26Z
file_id: '12443'
file_name: 2022_FrontiersImmunology_Dormeshkin.pdf
file_size: 5695892
relation: main_file
success: 1
file_date_updated: 2023-01-30T09:22:26Z
has_accepted_license: '1'
intvolume: ' 13'
isi: 1
keyword:
- Immunology
- Immunology and Allergy
- COVID-19
- SARS-CoV-2
- synthetic library
- RBD
- neutralization nanobody
- VHH
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: Frontiers in Immunology
publication_identifier:
issn:
- 1664-3224
publication_status: published
publisher: Frontiers Media
quality_controlled: '1'
scopus_import: '1'
status: public
title: Isolation of an escape-resistant SARS-CoV-2 neutralizing nanobody from a novel
synthetic nanobody library
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 13
year: '2022'
...
---
_id: '12261'
abstract:
- lang: eng
text: 'Dose–response relationships are a general concept for quantitatively describing
biological systems across multiple scales, from the molecular to the whole-cell
level. A clinically relevant example is the bacterial growth response to antibiotics,
which is routinely characterized by dose–response curves. The shape of the dose–response
curve varies drastically between antibiotics and plays a key role in treatment,
drug interactions, and resistance evolution. However, the mechanisms shaping the
dose–response curve remain largely unclear. Here, we show in Escherichia coli
that the distinctively shallow dose–response curve of the antibiotic trimethoprim
is caused by a negative growth-mediated feedback loop: Trimethoprim slows growth,
which in turn weakens the effect of this antibiotic. At the molecular level, this
feedback is caused by the upregulation of the drug target dihydrofolate reductase
(FolA/DHFR). We show that this upregulation is not a specific response to trimethoprim
but follows a universal trend line that depends primarily on the growth rate,
irrespective of its cause. Rewiring the feedback loop alters the dose–response
curve in a predictable manner, which we corroborate using a mathematical model
of cellular resource allocation and growth. Our results indicate that growth-mediated
feedback loops may shape drug responses more generally and could be exploited
to design evolutionary traps that enable selection against drug resistance.'
acknowledged_ssus:
- _id: M-Shop
acknowledgement: This work was in part supported by Human Frontier Science Program
GrantRGP0042/2013, Marie Curie Career Integration Grant303507, AustrianScience Fund
(FWF) Grant P27201-B22, and German Research Foundation(DFG) Collaborative Research
Center (SFB)1310to TB. SAA was supportedby the European Union’s Horizon2020Research
and Innovation Programunder the Marie Skłodowska-Curie Grant agreement No707352.
We wouldlike to thank the Bollenbach group for regular fruitful discussions. We
areparticularly thankful for the technical assistance of Booshini Fernando andfor
discussions of the theoretical aspects with Gerrit Ansmann. We areindebted to Bor
Kavˇciˇc for invaluable advice, help with setting up theluciferase-based growth
monitoring system, and for sharing plasmids. Weacknowledge the IST Austria Miba
Machine Shop for their support inbuilding a housing for the stacker of the plate
reader, which enabled thehigh-throughput luciferase-based experiments. We are grateful
to RosalindAllen, Bor Kavˇciˇc and Dor Russ for feedback on the manuscript. Open
Accessfunding enabled and organized by Projekt DEAL.
article_number: e10490
article_processing_charge: No
article_type: original
author:
- first_name: Andreas
full_name: Angermayr, Andreas
id: 4677C796-F248-11E8-B48F-1D18A9856A87
last_name: Angermayr
orcid: 0000-0001-8619-2223
- first_name: Tin Yau
full_name: Pang, Tin Yau
last_name: Pang
- first_name: Guillaume
full_name: Chevereau, Guillaume
last_name: Chevereau
- first_name: Karin
full_name: Mitosch, Karin
id: 39B66846-F248-11E8-B48F-1D18A9856A87
last_name: Mitosch
- first_name: Martin J
full_name: Lercher, Martin J
last_name: Lercher
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Angermayr A, Pang TY, Chevereau G, Mitosch K, Lercher MJ, Bollenbach MT. Growth‐mediated
negative feedback shapes quantitative antibiotic response. Molecular Systems
Biology. 2022;18(9). doi:10.15252/msb.202110490
apa: Angermayr, A., Pang, T. Y., Chevereau, G., Mitosch, K., Lercher, M. J., &
Bollenbach, M. T. (2022). Growth‐mediated negative feedback shapes quantitative
antibiotic response. Molecular Systems Biology. Embo Press. https://doi.org/10.15252/msb.202110490
chicago: Angermayr, Andreas, Tin Yau Pang, Guillaume Chevereau, Karin Mitosch, Martin
J Lercher, and Mark Tobias Bollenbach. “Growth‐mediated Negative Feedback Shapes
Quantitative Antibiotic Response.” Molecular Systems Biology. Embo Press,
2022. https://doi.org/10.15252/msb.202110490.
ieee: A. Angermayr, T. Y. Pang, G. Chevereau, K. Mitosch, M. J. Lercher, and M.
T. Bollenbach, “Growth‐mediated negative feedback shapes quantitative antibiotic
response,” Molecular Systems Biology, vol. 18, no. 9. Embo Press, 2022.
ista: Angermayr A, Pang TY, Chevereau G, Mitosch K, Lercher MJ, Bollenbach MT. 2022.
Growth‐mediated negative feedback shapes quantitative antibiotic response. Molecular
Systems Biology. 18(9), e10490.
mla: Angermayr, Andreas, et al. “Growth‐mediated Negative Feedback Shapes Quantitative
Antibiotic Response.” Molecular Systems Biology, vol. 18, no. 9, e10490,
Embo Press, 2022, doi:10.15252/msb.202110490.
short: A. Angermayr, T.Y. Pang, G. Chevereau, K. Mitosch, M.J. Lercher, M.T. Bollenbach,
Molecular Systems Biology 18 (2022).
date_created: 2023-01-16T09:58:34Z
date_published: 2022-09-01T00:00:00Z
date_updated: 2023-08-04T09:51:49Z
day: '01'
ddc:
- '570'
department:
- _id: ToBo
doi: 10.15252/msb.202110490
external_id:
isi:
- '000856482800001'
file:
- access_level: open_access
checksum: 8b1d8f5ea20c8408acf466435fb6ae01
content_type: application/pdf
creator: dernst
date_created: 2023-01-30T09:49:55Z
date_updated: 2023-01-30T09:49:55Z
file_id: '12446'
file_name: 2022_MolecularSystemsBio_Angermayr.pdf
file_size: 1098812
relation: main_file
success: 1
file_date_updated: 2023-01-30T09:49:55Z
has_accepted_license: '1'
intvolume: ' 18'
isi: 1
issue: '9'
keyword:
- Applied Mathematics
- Computational Theory and Mathematics
- General Agricultural and Biological Sciences
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- Information Systems
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: Molecular Systems Biology
publication_identifier:
eissn:
- 1744-4292
publication_status: published
publisher: Embo Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Growth‐mediated negative feedback shapes quantitative antibiotic response
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 18
year: '2022'
...
---
_id: '12288'
abstract:
- lang: eng
text: To understand the function of neuronal circuits, it is crucial to disentangle
the connectivity patterns within the network. However, most tools currently used
to explore connectivity have low throughput, low selectivity, or limited accessibility.
Here, we report the development of an improved packaging system for the production
of the highly neurotropic RVdGenvA-CVS-N2c rabies viral vectors, yielding titers
orders of magnitude higher with no background contamination, at a fraction of
the production time, while preserving the efficiency of transsynaptic labeling.
Along with the production pipeline, we developed suites of ‘starter’ AAV and bicistronic
RVdG-CVS-N2c vectors, enabling retrograde labeling from a wide range of neuronal
populations, tailored for diverse experimental requirements. We demonstrate the
power and flexibility of the new system by uncovering hidden local and distal
inhibitory connections in the mouse hippocampal formation and by imaging the functional
properties of a cortical microcircuit across weeks. Our novel production pipeline
provides a convenient approach to generate new rabies vectors, while our toolkit
flexibly and efficiently expands the current capacity to label, manipulate and
image the neuronal activity of interconnected neuronal circuits in vitro and in
vivo.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: We thank F Marr for technical assistance, A Murray for RVdG-CVS-N2c
viruses and Neuro2A packaging cell-lines and J Watson for reading the manuscript.
This research was supported by the Scientific Service Units (SSU) of IST-Austria
through resources provided by the Imaging and Optics Facility (IOF) and the Preclinical
Facility (PCF). This project was funded by the European Research Council (ERC) under
the European Union’s Horizon 2020 research and innovation programme (ERC advanced
grant No 692692, PJ, ERC starting grant No 756502, MJ), the Fond zur Förderung der
Wissenschaftlichen Forschung (Z 312-B27, Wittgenstein award, PJ), the Human Frontier
Science Program (LT000256/2018-L, AS) and EMBO (ALTF 1098-2017, AS).
article_number: '79848'
article_processing_charge: No
article_type: original
author:
- first_name: Anton L
full_name: Sumser, Anton L
id: 3320A096-F248-11E8-B48F-1D18A9856A87
last_name: Sumser
orcid: 0000-0002-4792-1881
- first_name: Maximilian A
full_name: Jösch, Maximilian A
id: 2BD278E6-F248-11E8-B48F-1D18A9856A87
last_name: Jösch
orcid: 0000-0002-3937-1330
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Yoav
full_name: Ben Simon, Yoav
id: 43DF3136-F248-11E8-B48F-1D18A9856A87
last_name: Ben Simon
citation:
ama: Sumser AL, Jösch MA, Jonas PM, Ben Simon Y. Fast, high-throughput production
of improved rabies viral vectors for specific, efficient and versatile transsynaptic
retrograde labeling. eLife. 2022;11. doi:10.7554/elife.79848
apa: Sumser, A. L., Jösch, M. A., Jonas, P. M., & Ben Simon, Y. (2022). Fast,
high-throughput production of improved rabies viral vectors for specific, efficient
and versatile transsynaptic retrograde labeling. ELife. eLife Sciences
Publications. https://doi.org/10.7554/elife.79848
chicago: Sumser, Anton L, Maximilian A Jösch, Peter M Jonas, and Yoav Ben Simon.
“Fast, High-Throughput Production of Improved Rabies Viral Vectors for Specific,
Efficient and Versatile Transsynaptic Retrograde Labeling.” ELife. eLife
Sciences Publications, 2022. https://doi.org/10.7554/elife.79848.
ieee: A. L. Sumser, M. A. Jösch, P. M. Jonas, and Y. Ben Simon, “Fast, high-throughput
production of improved rabies viral vectors for specific, efficient and versatile
transsynaptic retrograde labeling,” eLife, vol. 11. eLife Sciences Publications,
2022.
ista: Sumser AL, Jösch MA, Jonas PM, Ben Simon Y. 2022. Fast, high-throughput production
of improved rabies viral vectors for specific, efficient and versatile transsynaptic
retrograde labeling. eLife. 11, 79848.
mla: Sumser, Anton L., et al. “Fast, High-Throughput Production of Improved Rabies
Viral Vectors for Specific, Efficient and Versatile Transsynaptic Retrograde Labeling.”
ELife, vol. 11, 79848, eLife Sciences Publications, 2022, doi:10.7554/elife.79848.
short: A.L. Sumser, M.A. Jösch, P.M. Jonas, Y. Ben Simon, ELife 11 (2022).
date_created: 2023-01-16T10:04:15Z
date_published: 2022-09-15T00:00:00Z
date_updated: 2023-08-04T10:29:48Z
day: '15'
ddc:
- '570'
department:
- _id: MaJö
- _id: PeJo
doi: 10.7554/elife.79848
ec_funded: 1
external_id:
isi:
- '000892204300001'
pmid:
- '36040301'
file:
- access_level: open_access
checksum: 5a2a65e3e7225090c3d8199f3bbd7b7b
content_type: application/pdf
creator: dernst
date_created: 2023-01-30T11:50:53Z
date_updated: 2023-01-30T11:50:53Z
file_id: '12463'
file_name: 2022_eLife_Sumser.pdf
file_size: 8506811
relation: main_file
success: 1
file_date_updated: 2023-01-30T11:50:53Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '692692'
name: Biophysics and circuit function of a giant cortical glumatergic synapse
- _id: 2634E9D2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '756502'
name: Circuits of Visual Attention
- _id: 25C5A090-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z00312
name: The Wittgenstein Prize
- _id: 266D407A-B435-11E9-9278-68D0E5697425
grant_number: LT000256
name: Neuronal networks of salience and spatial detection in the murine superior
colliculus
- _id: 264FEA02-B435-11E9-9278-68D0E5697425
grant_number: ALTF 1098-2017
name: Connecting sensory with motor processing in the superior colliculus
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Fast, high-throughput production of improved rabies viral vectors for specific,
efficient and versatile transsynaptic retrograde labeling
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2022'
...
---
_id: '10836'
acknowledgement: This work was supported by the Austrian Science Fund (FWF) grants MCCA W1248-B30 and SFB F4606-B28 to EJJ. CP received a short-term
research fellowship of the European Federation of Immunological Societies (EFIS-IL) for a research visit at Biocruces Bizkaia Health Research Institute, Barakaldo, Spain. VKK received an EFIS-IL short-term research fellowship for a research visit at King’s College London. The
research was funded by the National Institute for Health Research (NIHR) Biomedical
Research Centre (BRC) based at Guy's and St Thomas' NHS Foundation Trust and King's
College London (IS-BRC-1215-20006) (SNK). The authors acknowledge support by the Medical Research Council
(MR/L023091/1) (SNK); Breast Cancer Now (147; KCL-BCN-Q3)(SNK); Cancer Research
UK (C30122/A11527; C30122/A15774) (SNK); Cancer Research UK King's Health Partners Centre at King's College London (C604/A25135) (SNK); CRUK/NIHR in England/DoH for Scotland, Wales and Northern Ireland Experimental Cancer Medicine Centre (C10355/A15587) (SNK). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. Additionally, this work was funded by Instituto de Salud Carlos III through the project "PI16/01223" (Co-funded by European
Regional Development Fund; “A way to make Europe”) to FB and by the Department of Health, Basque Government through the project
“2019111031” to OZ. OZ is recipient of a Sara Borrell 2017 post-doctoral contract
“CD17/00128” funded by Instituto de Salud Carlos III (Co-funded by European Social
Fund; “Investing in your future”).
article_processing_charge: No
article_type: letter_note
author:
- first_name: Christina L.
full_name: Pranger, Christina L.
last_name: Pranger
- first_name: Judit
full_name: Fazekas-Singer, Judit
id: 36432834-F248-11E8-B48F-1D18A9856A87
last_name: Fazekas-Singer
orcid: 0000-0002-8777-3502
- first_name: Verena K.
full_name: Köhler, Verena K.
last_name: Köhler
- first_name: Isabella
full_name: Pali‐Schöll, Isabella
last_name: Pali‐Schöll
- first_name: Alessandro
full_name: Fiocchi, Alessandro
last_name: Fiocchi
- first_name: Sophia N.
full_name: Karagiannis, Sophia N.
last_name: Karagiannis
- first_name: Olatz
full_name: Zenarruzabeitia, Olatz
last_name: Zenarruzabeitia
- first_name: Francisco
full_name: Borrego, Francisco
last_name: Borrego
- first_name: Erika
full_name: Jensen‐Jarolim, Erika
last_name: Jensen‐Jarolim
citation:
ama: 'Pranger CL, Singer J, Köhler VK, et al. PIPE‐cloned human IgE and IgG4 antibodies:
New tools for investigating cow’s milk allergy and tolerance. Allergy.
2021;76(5):1553-1556. doi:10.1111/all.14604'
apa: 'Pranger, C. L., Singer, J., Köhler, V. K., Pali‐Schöll, I., Fiocchi, A., Karagiannis,
S. N., … Jensen‐Jarolim, E. (2021). PIPE‐cloned human IgE and IgG4 antibodies:
New tools for investigating cow’s milk allergy and tolerance. Allergy.
Wiley. https://doi.org/10.1111/all.14604'
chicago: 'Pranger, Christina L., Judit Singer, Verena K. Köhler, Isabella Pali‐Schöll,
Alessandro Fiocchi, Sophia N. Karagiannis, Olatz Zenarruzabeitia, Francisco Borrego,
and Erika Jensen‐Jarolim. “PIPE‐cloned Human IgE and IgG4 Antibodies: New Tools
for Investigating Cow’s Milk Allergy and Tolerance.” Allergy. Wiley, 2021.
https://doi.org/10.1111/all.14604.'
ieee: 'C. L. Pranger et al., “PIPE‐cloned human IgE and IgG4 antibodies:
New tools for investigating cow’s milk allergy and tolerance,” Allergy,
vol. 76, no. 5. Wiley, pp. 1553–1556, 2021.'
ista: 'Pranger CL, Singer J, Köhler VK, Pali‐Schöll I, Fiocchi A, Karagiannis SN,
Zenarruzabeitia O, Borrego F, Jensen‐Jarolim E. 2021. PIPE‐cloned human IgE and
IgG4 antibodies: New tools for investigating cow’s milk allergy and tolerance.
Allergy. 76(5), 1553–1556.'
mla: 'Pranger, Christina L., et al. “PIPE‐cloned Human IgE and IgG4 Antibodies:
New Tools for Investigating Cow’s Milk Allergy and Tolerance.” Allergy,
vol. 76, no. 5, Wiley, 2021, pp. 1553–56, doi:10.1111/all.14604.'
short: C.L. Pranger, J. Singer, V.K. Köhler, I. Pali‐Schöll, A. Fiocchi, S.N. Karagiannis,
O. Zenarruzabeitia, F. Borrego, E. Jensen‐Jarolim, Allergy 76 (2021) 1553–1556.
date_created: 2022-03-08T11:19:05Z
date_published: 2021-05-01T00:00:00Z
date_updated: 2023-09-05T15:58:53Z
day: '01'
ddc:
- '570'
department:
- _id: Bio
doi: 10.1111/all.14604
external_id:
isi:
- '000577708800001'
pmid:
- '32990982'
file:
- access_level: open_access
checksum: 9526f9554112fc027c9f7fa540c488cd
content_type: application/pdf
creator: dernst
date_created: 2022-03-08T11:23:16Z
date_updated: 2022-03-08T11:23:16Z
file_id: '10837'
file_name: 2021_Allergy_Pranger.pdf
file_size: 626081
relation: main_file
success: 1
file_date_updated: 2022-03-08T11:23:16Z
has_accepted_license: '1'
intvolume: ' 76'
isi: 1
issue: '5'
keyword:
- Immunology
- Immunology and Allergy
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 1553-1556
pmid: 1
publication: Allergy
publication_identifier:
eissn:
- 1398-9995
issn:
- 0105-4538
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'PIPE‐cloned human IgE and IgG4 antibodies: New tools for investigating cow''s
milk allergy and tolerance'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 76
year: '2021'
...
---
_id: '9387'
abstract:
- lang: eng
text: We report the complete analysis of a deterministic model of deleterious mutations
and negative selection against them at two haploid loci without recombination.
As long as mutation is a weaker force than selection, mutant alleles remain rare
at the only stable equilibrium, and otherwise, a variety of dynamics are possible.
If the mutation-free genotype is absent, generally the only stable equilibrium
is the one that corresponds to fixation of the mutant allele at the locus where
it is less deleterious. This result suggests that fixation of a deleterious allele
that follows a click of the Muller’s ratchet is governed by natural selection,
instead of random drift.
acknowledgement: This work was supported by the Russian Science Foundation grant N
16-14-10173.
article_number: '110729'
article_processing_charge: No
article_type: original
author:
- first_name: Kseniia
full_name: Khudiakova, Kseniia
id: 4E6DC800-AE37-11E9-AC72-31CAE5697425
last_name: Khudiakova
orcid: 0000-0002-6246-1465
- first_name: Tatiana Yu.
full_name: Neretina, Tatiana Yu.
last_name: Neretina
- first_name: Alexey S.
full_name: Kondrashov, Alexey S.
last_name: Kondrashov
citation:
ama: Khudiakova K, Neretina TY, Kondrashov AS. Two linked loci under mutation-selection
balance and Muller’s ratchet. Journal of Theoretical Biology. 2021;524.
doi:10.1016/j.jtbi.2021.110729
apa: Khudiakova, K., Neretina, T. Y., & Kondrashov, A. S. (2021). Two linked
loci under mutation-selection balance and Muller’s ratchet. Journal of Theoretical
Biology. Elsevier . https://doi.org/10.1016/j.jtbi.2021.110729
chicago: Khudiakova, Kseniia, Tatiana Yu. Neretina, and Alexey S. Kondrashov. “Two
Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” Journal
of Theoretical Biology. Elsevier , 2021. https://doi.org/10.1016/j.jtbi.2021.110729.
ieee: K. Khudiakova, T. Y. Neretina, and A. S. Kondrashov, “Two linked loci under
mutation-selection balance and Muller’s ratchet,” Journal of Theoretical Biology,
vol. 524. Elsevier , 2021.
ista: Khudiakova K, Neretina TY, Kondrashov AS. 2021. Two linked loci under mutation-selection
balance and Muller’s ratchet. Journal of Theoretical Biology. 524, 110729.
mla: Khudiakova, Kseniia, et al. “Two Linked Loci under Mutation-Selection Balance
and Muller’s Ratchet.” Journal of Theoretical Biology, vol. 524, 110729,
Elsevier , 2021, doi:10.1016/j.jtbi.2021.110729.
short: K. Khudiakova, T.Y. Neretina, A.S. Kondrashov, Journal of Theoretical Biology
524 (2021).
date_created: 2021-05-12T05:58:42Z
date_published: 2021-04-24T00:00:00Z
date_updated: 2023-08-08T13:32:40Z
day: '24'
department:
- _id: GradSch
doi: 10.1016/j.jtbi.2021.110729
external_id:
isi:
- '000659161500002'
intvolume: ' 524'
isi: 1
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- Modelling and Simulation
- Statistics and Probability
- General Immunology and Microbiology
- Applied Mathematics
- General Agricultural and Biological Sciences
- General Medicine
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.biorxiv.org/content/10.1101/477489v1
month: '04'
oa: 1
oa_version: Preprint
publication: Journal of Theoretical Biology
publication_identifier:
issn:
- 0022-5193
publication_status: published
publisher: 'Elsevier '
quality_controlled: '1'
status: public
title: Two linked loci under mutation-selection balance and Muller’s ratchet
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 524
year: '2021'
...
---
_id: '10301'
abstract:
- lang: eng
text: De novo protein synthesis is required for synapse modifications underlying
stable memory encoding. Yet neurons are highly compartmentalized cells and how
protein synthesis can be regulated at the synapse level is unknown. Here, we characterize
neuronal signaling complexes formed by the postsynaptic scaffold GIT1, the mechanistic
target of rapamycin (mTOR) kinase, and Raptor that couple synaptic stimuli to
mTOR-dependent protein synthesis; and identify NMDA receptors containing GluN3A
subunits as key negative regulators of GIT1 binding to mTOR. Disruption of GIT1/mTOR
complexes by enhancing GluN3A expression or silencing GIT1 inhibits synaptic mTOR
activation and restricts the mTOR-dependent translation of specific activity-regulated
mRNAs. Conversely, GluN3A removal enables complex formation, potentiates mTOR-dependent
protein synthesis, and facilitates the consolidation of associative and spatial
memories in mice. The memory enhancement becomes evident with light or spaced
training, can be achieved by selectively deleting GluN3A from excitatory neurons
during adulthood, and does not compromise other aspects of cognition such as memory
flexibility or extinction. Our findings provide mechanistic insight into synaptic
translational control and reveal a potentially selective target for cognitive
enhancement.
acknowledgement: We thank Stuart Lipton and Nobuki Nakanishi for providing the Grin3a
knockout mice, Beverly Davidson for the AAV-caRheb, Jose Esteban for help with behavioral
and biochemical experiments, and Noelia Campillo, Rebeca Martínez-Turrillas, and
Ana Navarro for expert technical help. Work was funded by the UTE project CIMA;
fellowships from the Fundación Tatiana Pérez de Guzmán el Bueno, FEBS, and IBRO
(to M.J.C.D.), Generalitat Valenciana (to O.E.-Z.), Juan de la Cierva (to L.G.R.),
FPI-MINECO (to E.R.V., to S.N.) and Intertalentum postdoctoral program (to V.B.);
ANR (GluBrain3A) and ERC Advanced Grants (#693021) (to P.P.); Ramón y Cajal program
RYC2014-15784, RETOS-MINECO SAF2016-76565-R, ERANET-Neuron JTC 2019 ISCIII AC19/00077
FEDER funds (to R.A.); RETOS-MINECO SAF2017-87928-R (to A.B.); an NIH grant (NS76637)
and UTHSC College of Medicine funds (to S.J.T.); and NARSAD Independent Investigator
Award and grants from the MINECO (CSD2008-00005, SAF2013-48983R, SAF2016-80895-R),
Generalitat Valenciana (PROMETEO 2019/020)(to I.P.O.) and Severo-Ochoa Excellence
Awards (SEV-2013-0317, SEV-2017-0723).
article_number: e71575
article_processing_charge: No
article_type: original
author:
- first_name: María J
full_name: Conde-Dusman, María J
last_name: Conde-Dusman
- first_name: Partha N
full_name: Dey, Partha N
last_name: Dey
- first_name: Óscar
full_name: Elía-Zudaire, Óscar
last_name: Elía-Zudaire
- first_name: Luis E
full_name: Garcia Rabaneda, Luis E
id: 33D1B084-F248-11E8-B48F-1D18A9856A87
last_name: Garcia Rabaneda
- first_name: Carmen
full_name: García-Lira, Carmen
last_name: García-Lira
- first_name: Teddy
full_name: Grand, Teddy
last_name: Grand
- first_name: Victor
full_name: Briz, Victor
last_name: Briz
- first_name: Eric R
full_name: Velasco, Eric R
last_name: Velasco
- first_name: Raül
full_name: Andero Galí, Raül
last_name: Andero Galí
- first_name: Sergio
full_name: Niñerola, Sergio
last_name: Niñerola
- first_name: Angel
full_name: Barco, Angel
last_name: Barco
- first_name: Pierre
full_name: Paoletti, Pierre
last_name: Paoletti
- first_name: John F
full_name: Wesseling, John F
last_name: Wesseling
- first_name: Fabrizio
full_name: Gardoni, Fabrizio
last_name: Gardoni
- first_name: Steven J
full_name: Tavalin, Steven J
last_name: Tavalin
- first_name: Isabel
full_name: Perez-Otaño, Isabel
last_name: Perez-Otaño
citation:
ama: Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, et al. Control of protein synthesis
and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly.
eLife. 2021;10. doi:10.7554/elife.71575
apa: Conde-Dusman, M. J., Dey, P. N., Elía-Zudaire, Ó., Garcia Rabaneda, L. E.,
García-Lira, C., Grand, T., … Perez-Otaño, I. (2021). Control of protein synthesis
and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly.
ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.71575
chicago: Conde-Dusman, María J, Partha N Dey, Óscar Elía-Zudaire, Luis E Garcia
Rabaneda, Carmen García-Lira, Teddy Grand, Victor Briz, et al. “Control of Protein
Synthesis and Memory by GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1
Assembly.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/elife.71575.
ieee: M. J. Conde-Dusman et al., “Control of protein synthesis and memory
by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly,” eLife,
vol. 10. eLife Sciences Publications, 2021.
ista: Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, Garcia Rabaneda LE, García-Lira C,
Grand T, Briz V, Velasco ER, Andero Galí R, Niñerola S, Barco A, Paoletti P, Wesseling
JF, Gardoni F, Tavalin SJ, Perez-Otaño I. 2021. Control of protein synthesis and
memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. eLife.
10, e71575.
mla: Conde-Dusman, María J., et al. “Control of Protein Synthesis and Memory by
GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1 Assembly.” ELife,
vol. 10, e71575, eLife Sciences Publications, 2021, doi:10.7554/elife.71575.
short: M.J. Conde-Dusman, P.N. Dey, Ó. Elía-Zudaire, L.E. Garcia Rabaneda, C. García-Lira,
T. Grand, V. Briz, E.R. Velasco, R. Andero Galí, S. Niñerola, A. Barco, P. Paoletti,
J.F. Wesseling, F. Gardoni, S.J. Tavalin, I. Perez-Otaño, ELife 10 (2021).
date_created: 2021-11-18T06:59:45Z
date_published: 2021-11-17T00:00:00Z
date_updated: 2023-08-14T11:50:50Z
day: '17'
ddc:
- '570'
department:
- _id: GaNo
doi: 10.7554/elife.71575
external_id:
isi:
- '000720945900001'
file:
- access_level: open_access
checksum: 59318e9e41507cec83c2f4070e6ad540
content_type: application/pdf
creator: lgarciar
date_created: 2021-11-18T07:02:02Z
date_updated: 2021-11-18T07:02:02Z
file_id: '10302'
file_name: elife-71575-v1.pdf
file_size: 2477302
relation: main_file
success: 1
file_date_updated: 2021-11-18T07:02:02Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
keyword:
- general immunology and microbiology
- general biochemistry
- genetics and molecular biology
- general medicine
- general neuroscience
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
status: public
title: Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition
of GIT1/mTORC1 assembly
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 10
year: '2021'
...
---
_id: '11055'
abstract:
- lang: eng
text: Vascular dysfunctions are a common feature of multiple age-related diseases.
However, modeling healthy and pathological aging of the human vasculature represents
an unresolved experimental challenge. Here, we generated induced vascular endothelial
cells (iVECs) and smooth muscle cells (iSMCs) by direct reprogramming of healthy
human fibroblasts from donors of different ages and Hutchinson-Gilford Progeria
Syndrome (HGPS) patients. iVECs induced from old donors revealed upregulation
of GSTM1 and PALD1, genes linked to oxidative stress, inflammation and endothelial
junction stability, as vascular aging markers. A functional assay performed on
PALD1 KD VECs demonstrated a recovery in vascular permeability. We found that
iSMCs from HGPS donors overexpressed bone morphogenetic protein (BMP)−4, which
plays a key role in both vascular calcification and endothelial barrier damage
observed in HGPS. Strikingly, BMP4 concentrations are higher in serum from HGPS
vs. age-matched mice. Furthermore, targeting BMP4 with blocking antibody recovered
the functionality of the vascular barrier in vitro, hence representing a potential
future therapeutic strategy to limit cardiovascular dysfunction in HGPS. These
results show that iVECs and iSMCs retain disease-related signatures, allowing
modeling of vascular aging and HGPS in vitro.
article_number: e54383
article_processing_charge: No
article_type: original
author:
- first_name: Simone
full_name: Bersini, Simone
last_name: Bersini
- first_name: Roberta
full_name: Schulte, Roberta
last_name: Schulte
- first_name: Ling
full_name: Huang, Ling
last_name: Huang
- first_name: Hannah
full_name: Tsai, Hannah
last_name: Tsai
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Bersini S, Schulte R, Huang L, Tsai H, Hetzer M. Direct reprogramming of human
smooth muscle and vascular endothelial cells reveals defects associated with aging
and Hutchinson-Gilford progeria syndrome. eLife. 2020;9. doi:10.7554/elife.54383
apa: Bersini, S., Schulte, R., Huang, L., Tsai, H., & Hetzer, M. (2020). Direct
reprogramming of human smooth muscle and vascular endothelial cells reveals defects
associated with aging and Hutchinson-Gilford progeria syndrome. ELife.
eLife Sciences Publications. https://doi.org/10.7554/elife.54383
chicago: Bersini, Simone, Roberta Schulte, Ling Huang, Hannah Tsai, and Martin Hetzer.
“Direct Reprogramming of Human Smooth Muscle and Vascular Endothelial Cells Reveals
Defects Associated with Aging and Hutchinson-Gilford Progeria Syndrome.” ELife.
eLife Sciences Publications, 2020. https://doi.org/10.7554/elife.54383.
ieee: S. Bersini, R. Schulte, L. Huang, H. Tsai, and M. Hetzer, “Direct reprogramming
of human smooth muscle and vascular endothelial cells reveals defects associated
with aging and Hutchinson-Gilford progeria syndrome,” eLife, vol. 9. eLife
Sciences Publications, 2020.
ista: Bersini S, Schulte R, Huang L, Tsai H, Hetzer M. 2020. Direct reprogramming
of human smooth muscle and vascular endothelial cells reveals defects associated
with aging and Hutchinson-Gilford progeria syndrome. eLife. 9, e54383.
mla: Bersini, Simone, et al. “Direct Reprogramming of Human Smooth Muscle and Vascular
Endothelial Cells Reveals Defects Associated with Aging and Hutchinson-Gilford
Progeria Syndrome.” ELife, vol. 9, e54383, eLife Sciences Publications,
2020, doi:10.7554/elife.54383.
short: S. Bersini, R. Schulte, L. Huang, H. Tsai, M. Hetzer, ELife 9 (2020).
date_created: 2022-04-07T07:43:48Z
date_published: 2020-09-08T00:00:00Z
date_updated: 2022-07-18T08:30:37Z
day: '08'
ddc:
- '570'
doi: 10.7554/elife.54383
extern: '1'
external_id:
pmid:
- '32896271'
file:
- access_level: open_access
checksum: f8b3821349a194050be02570d8fe7d4b
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T06:53:10Z
date_updated: 2022-04-08T06:53:10Z
file_id: '11132'
file_name: 2020_eLife_Bersini.pdf
file_size: 4399825
relation: main_file
success: 1
file_date_updated: 2022-04-08T06:53:10Z
has_accepted_license: '1'
intvolume: ' 9'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Direct reprogramming of human smooth muscle and vascular endothelial cells
reveals defects associated with aging and Hutchinson-Gilford progeria syndrome
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 9
year: '2020'
...
---
_id: '11060'
abstract:
- lang: eng
text: The inner nuclear membrane (INM) is a subdomain of the endoplasmic reticulum
(ER) that is gated by the nuclear pore complex. It is unknown whether proteins
of the INM and ER are degraded through shared or distinct pathways in mammalian
cells. We applied dynamic proteomics to profile protein half-lives and report
that INM and ER residents turn over at similar rates, indicating that the INM’s
unique topology is not a barrier to turnover. Using a microscopy approach, we
observed that the proteasome can degrade INM proteins in situ. However, we also
uncovered evidence for selective, vesicular transport-mediated turnover of a single
INM protein, emerin, that is potentiated by ER stress. Emerin is rapidly cleared
from the INM by a mechanism that requires emerin’s LEM domain to mediate vesicular
trafficking to lysosomes. This work demonstrates that the INM can be dynamically
remodeled in response to environmental inputs.
article_number: e49796
article_processing_charge: No
article_type: original
author:
- first_name: Abigail
full_name: Buchwalter, Abigail
last_name: Buchwalter
- first_name: Roberta
full_name: Schulte, Roberta
last_name: Schulte
- first_name: Hsiao
full_name: Tsai, Hsiao
last_name: Tsai
- first_name: Juliana
full_name: Capitanio, Juliana
last_name: Capitanio
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
citation:
ama: Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. Selective clearance
of the inner nuclear membrane protein emerin by vesicular transport during ER
stress. eLife. 2019;8. doi:10.7554/elife.49796
apa: Buchwalter, A., Schulte, R., Tsai, H., Capitanio, J., & Hetzer, M. (2019).
Selective clearance of the inner nuclear membrane protein emerin by vesicular
transport during ER stress. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.49796
chicago: Buchwalter, Abigail, Roberta Schulte, Hsiao Tsai, Juliana Capitanio, and
Martin Hetzer. “Selective Clearance of the Inner Nuclear Membrane Protein Emerin
by Vesicular Transport during ER Stress.” ELife. eLife Sciences Publications,
2019. https://doi.org/10.7554/elife.49796.
ieee: A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, and M. Hetzer, “Selective
clearance of the inner nuclear membrane protein emerin by vesicular transport
during ER stress,” eLife, vol. 8. eLife Sciences Publications, 2019.
ista: Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. 2019. Selective clearance
of the inner nuclear membrane protein emerin by vesicular transport during ER
stress. eLife. 8, e49796.
mla: Buchwalter, Abigail, et al. “Selective Clearance of the Inner Nuclear Membrane
Protein Emerin by Vesicular Transport during ER Stress.” ELife, vol. 8,
e49796, eLife Sciences Publications, 2019, doi:10.7554/elife.49796.
short: A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, M. Hetzer, ELife 8 (2019).
date_created: 2022-04-07T07:45:02Z
date_published: 2019-10-10T00:00:00Z
date_updated: 2023-05-31T06:36:22Z
day: '10'
ddc:
- '570'
doi: 10.7554/elife.49796
extern: '1'
external_id:
pmid:
- '31599721'
file:
- access_level: open_access
checksum: 1e8672a1e9c3dc0a2d3d0dad89673616
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T08:18:01Z
date_updated: 2022-04-08T08:18:01Z
file_id: '11138'
file_name: 2019_eLife_Buchwalter.pdf
file_size: 6984654
relation: main_file
success: 1
file_date_updated: 2022-04-08T08:18:01Z
has_accepted_license: '1'
intvolume: ' 8'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Medicine
- General Neuroscience
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
related_material:
record:
- id: '13079'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Selective clearance of the inner nuclear membrane protein emerin by vesicular
transport during ER stress
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 8
year: '2019'
...
---
_id: '6891'
abstract:
- lang: eng
text: "While cells of mesenchymal or epithelial origin perform their effector functions
in a purely anchorage dependent manner, cells derived from the hematopoietic lineage
are not committed to operate only within a specific niche. Instead, these cells
are able to function autonomously of the molecular composition in a broad range
of tissue compartments. By this means, cells of the hematopoietic lineage retain
the capacity to disseminate into connective tissue and recirculate between organs,
building the foundation for essential processes such as tissue regeneration or
immune surveillance. \r\nCells of the immune system, specifically leukocytes,
are extraordinarily good at performing this task. These cells are able to flexibly
shift their mode of migration between an adhesion-mediated and an adhesion-independent
manner, instantaneously accommodating for any changes in molecular composition
of the external scaffold. The key component driving directed leukocyte migration
is the chemokine receptor 7, which guides the cell along gradients of chemokine
ligand. Therefore, the physical destination of migrating leukocytes is purely
deterministic, i.e. given by global directional cues such as chemokine gradients.
\r\nNevertheless, these cells typically reside in three-dimensional scaffolds
of inhomogeneous complexity, raising the question whether cells are able to locally
discriminate between multiple optional migration routes. Current literature provides
evidence that leukocytes, specifically dendritic cells, do indeed probe their
surrounding by virtue of multiple explorative protrusions. However, it remains
enigmatic how these cells decide which one is the more favorable route to follow
and what are the key players involved in performing this task. Due to the heterogeneous
environment of most tissues, and the vast adaptability of migrating leukocytes,
at this time it is not clear to what extent leukocytes are able to optimize their
migratory strategy by adapting their level of adhesiveness. And, given the fact
that leukocyte migration is characterized by branched cell shapes in combination
with high migration velocities, it is reasonable to assume that these cells require
fine tuned shape maintenance mechanisms that tightly coordinate protrusion and
adhesion dynamics in a spatiotemporal manner. \r\nTherefore, this study aimed
to elucidate how rapidly migrating leukocytes opt for an ideal migratory path
while maintaining a continuous cell shape and balancing adhesive forces to efficiently
navigate through complex microenvironments. \r\nThe results of this study unraveled
a role for the microtubule cytoskeleton in promoting the decision making process
during path finding and for the first time point towards a microtubule-mediated
function in cell shape maintenance of highly ramified cells such as dendritic
cells. Furthermore, we found that migrating low-adhesive leukocytes are able to
instantaneously adapt to increased tensile load by engaging adhesion receptors.
This response was only occurring tangential to the substrate while adhesive properties
in the vertical direction were not increased. As leukocytes are primed for rapid
migration velocities, these results demonstrate that leukocyte integrins are able
to confer a high level of traction forces parallel to the cell membrane along
the direction of migration without wasting energy in gluing the cell to the substrate.
\r\nThus, the data in the here presented thesis provide new insights into the
pivotal role of cytoskeletal dynamics and the mechanisms of force transduction
during leukocyte migration. \r\nThereby the here presented results help to further
define fundamental principles underlying leukocyte migration and open up potential
therapeutic avenues of clinical relevance.\r\n"
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
citation:
ama: Kopf A. The implication of cytoskeletal dynamics on leukocyte migration. 2019.
doi:10.15479/AT:ISTA:6891
apa: Kopf, A. (2019). The implication of cytoskeletal dynamics on leukocyte migration.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:6891
chicago: Kopf, Aglaja. “The Implication of Cytoskeletal Dynamics on Leukocyte Migration.”
Institute of Science and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6891.
ieee: A. Kopf, “The implication of cytoskeletal dynamics on leukocyte migration,”
Institute of Science and Technology Austria, 2019.
ista: Kopf A. 2019. The implication of cytoskeletal dynamics on leukocyte migration.
Institute of Science and Technology Austria.
mla: Kopf, Aglaja. The Implication of Cytoskeletal Dynamics on Leukocyte Migration.
Institute of Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:6891.
short: A. Kopf, The Implication of Cytoskeletal Dynamics on Leukocyte Migration,
Institute of Science and Technology Austria, 2019.
date_created: 2019-09-19T08:19:44Z
date_published: 2019-07-24T00:00:00Z
date_updated: 2023-10-18T08:49:17Z
day: '24'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:6891
file:
- access_level: closed
checksum: 00d100d6468e31e583051e0a006b640c
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: akopf
date_created: 2019-10-15T05:28:42Z
date_updated: 2020-10-17T22:30:03Z
embargo_to: open_access
file_id: '6950'
file_name: Kopf_PhD_Thesis.docx
file_size: 74735267
relation: source_file
- access_level: open_access
checksum: 5d1baa899993ae6ca81aebebe1797000
content_type: application/pdf
creator: akopf
date_created: 2019-10-15T05:28:47Z
date_updated: 2020-10-17T22:30:03Z
embargo: 2020-10-16
file_id: '6951'
file_name: Kopf_PhD_Thesis1.pdf
file_size: 52787224
relation: main_file
file_date_updated: 2020-10-17T22:30:03Z
has_accepted_license: '1'
keyword:
- cell biology
- immunology
- leukocyte
- migration
- microfluidics
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: '171'
project:
- _id: 265E2996-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W01250-B20
name: Nano-Analytics of Cellular Systems
publication_identifier:
eissn:
- 2663-337X
isbn:
- 978-3-99078-002-2
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
link:
- relation: press_release
url: https://ist.ac.at/en/news/feeling-like-a-cell/
record:
- id: '6328'
relation: part_of_dissertation
status: public
- id: '15'
relation: part_of_dissertation
status: public
- id: '6877'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: The implication of cytoskeletal dynamics on leukocyte migration
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2019'
...