---
_id: '10834'
abstract:
- lang: eng
text: Hematopoietic-specific protein 1 (Hem1) is an essential subunit of the WAVE
regulatory complex (WRC) in immune cells. WRC is crucial for Arp2/3 complex activation
and the protrusion of branched actin filament networks. Moreover, Hem1 loss of
function in immune cells causes autoimmune diseases in humans. Here, we show that
genetic removal of Hem1 in macrophages diminishes frequency and efficacy of phagocytosis
as well as phagocytic cup formation in addition to defects in lamellipodial protrusion
and migration. Moreover, Hem1-null macrophages displayed strong defects in cell
adhesion despite unaltered podosome formation and concomitant extracellular matrix
degradation. Specifically, dynamics of both adhesion and de-adhesion as well as
concomitant phosphorylation of paxillin and focal adhesion kinase (FAK) were significantly
compromised. Accordingly, disruption of WRC function in non-hematopoietic cells
coincided with both defects in adhesion turnover and altered FAK and paxillin
phosphorylation. Consistently, platelets exhibited reduced adhesion and diminished
integrin αIIbβ3 activation upon WRC removal. Interestingly, adhesion phenotypes,
but not lamellipodia formation, were partially rescued by small molecule activation
of FAK. A full rescue of the phenotype, including lamellipodia formation, required
not only the presence of WRCs but also their binding to and activation by Rac.
Collectively, our results uncover that WRC impacts on integrin-dependent processes
in a FAK-dependent manner, controlling formation and dismantling of adhesions,
relevant for properly grabbing onto extracellular surfaces and particles during
cell edge expansion, like in migration or phagocytosis.
acknowledgement: We are grateful to Silvia Prettin, Ina Schleicher, and Petra Hagendorff
for expert technical assistance; David Dettbarn for animal keeping and breeding;
and Lothar Gröbe and Maria Höxter for cell sorting. We also thank Werner Tegge for
peptides and Giorgio Scita for antibodies. This work was supported, in part, by
the Deutsche Forschungsgemeinschaft (DFG), Priority Programm SPP1150 (to T.E.B.S.,
K.R., and M. Sixt), and by DFG grant GRK2223/1 (to K.R.). T.E.B.S. acknowledges
support by the Helmholtz Society through HGF impulse fund W2/W3-066 and M. Schnoor
by the Mexican Council for Science and Technology (CONACyT, 284292 ), Fund SEP-Cinvestav
( 108 ), and the Royal Society, UK (Newton Advanced Fellowship, NAF/R1/180017 ).
article_processing_charge: No
article_type: original
author:
- first_name: Stephanie
full_name: Stahnke, Stephanie
last_name: Stahnke
- first_name: Hermann
full_name: Döring, Hermann
last_name: Döring
- first_name: Charly
full_name: Kusch, Charly
last_name: Kusch
- first_name: David J.J.
full_name: de Gorter, David J.J.
last_name: de Gorter
- first_name: Sebastian
full_name: Dütting, Sebastian
last_name: Dütting
- first_name: Aleks
full_name: Guledani, Aleks
last_name: Guledani
- first_name: Irina
full_name: Pleines, Irina
last_name: Pleines
- first_name: Michael
full_name: Schnoor, Michael
last_name: Schnoor
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Robert
full_name: Geffers, Robert
last_name: Geffers
- first_name: Manfred
full_name: Rohde, Manfred
last_name: Rohde
- first_name: Mathias
full_name: Müsken, Mathias
last_name: Müsken
- first_name: Frieda
full_name: Kage, Frieda
last_name: Kage
- first_name: Anika
full_name: Steffen, Anika
last_name: Steffen
- first_name: Jan
full_name: Faix, Jan
last_name: Faix
- first_name: Bernhard
full_name: Nieswandt, Bernhard
last_name: Nieswandt
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Theresia E.B.
full_name: Stradal, Theresia E.B.
last_name: Stradal
citation:
ama: Stahnke S, Döring H, Kusch C, et al. Loss of Hem1 disrupts macrophage function
and impacts migration, phagocytosis, and integrin-mediated adhesion. Current
Biology. 2021;31(10):2051-2064.e8. doi:10.1016/j.cub.2021.02.043
apa: Stahnke, S., Döring, H., Kusch, C., de Gorter, D. J. J., Dütting, S., Guledani,
A., … Stradal, T. E. B. (2021). Loss of Hem1 disrupts macrophage function and
impacts migration, phagocytosis, and integrin-mediated adhesion. Current Biology.
Elsevier. https://doi.org/10.1016/j.cub.2021.02.043
chicago: Stahnke, Stephanie, Hermann Döring, Charly Kusch, David J.J. de Gorter,
Sebastian Dütting, Aleks Guledani, Irina Pleines, et al. “Loss of Hem1 Disrupts
Macrophage Function and Impacts Migration, Phagocytosis, and Integrin-Mediated
Adhesion.” Current Biology. Elsevier, 2021. https://doi.org/10.1016/j.cub.2021.02.043.
ieee: S. Stahnke et al., “Loss of Hem1 disrupts macrophage function and impacts
migration, phagocytosis, and integrin-mediated adhesion,” Current Biology,
vol. 31, no. 10. Elsevier, p. 2051–2064.e8, 2021.
ista: Stahnke S, Döring H, Kusch C, de Gorter DJJ, Dütting S, Guledani A, Pleines
I, Schnoor M, Sixt MK, Geffers R, Rohde M, Müsken M, Kage F, Steffen A, Faix J,
Nieswandt B, Rottner K, Stradal TEB. 2021. Loss of Hem1 disrupts macrophage function
and impacts migration, phagocytosis, and integrin-mediated adhesion. Current Biology.
31(10), 2051–2064.e8.
mla: Stahnke, Stephanie, et al. “Loss of Hem1 Disrupts Macrophage Function and Impacts
Migration, Phagocytosis, and Integrin-Mediated Adhesion.” Current Biology,
vol. 31, no. 10, Elsevier, 2021, p. 2051–2064.e8, doi:10.1016/j.cub.2021.02.043.
short: S. Stahnke, H. Döring, C. Kusch, D.J.J. de Gorter, S. Dütting, A. Guledani,
I. Pleines, M. Schnoor, M.K. Sixt, R. Geffers, M. Rohde, M. Müsken, F. Kage, A.
Steffen, J. Faix, B. Nieswandt, K. Rottner, T.E.B. Stradal, Current Biology 31
(2021) 2051–2064.e8.
date_created: 2022-03-08T07:51:04Z
date_published: 2021-05-24T00:00:00Z
date_updated: 2023-08-17T07:01:14Z
day: '24'
department:
- _id: MiSi
doi: 10.1016/j.cub.2021.02.043
external_id:
isi:
- '000654652200002'
pmid:
- '33711252'
intvolume: ' 31'
isi: 1
issue: '10'
keyword:
- General Agricultural and Biological Sciences
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2020.03.24.005835
month: '05'
oa: 1
oa_version: Preprint
page: 2051-2064.e8
pmid: 1
publication: Current Biology
publication_identifier:
issn:
- 0960-9822
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis,
and integrin-mediated adhesion
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 31
year: '2021'
...
---
_id: '11052'
abstract:
- lang: eng
text: In order to combat molecular damage, most cellular proteins undergo rapid
turnover. We have previously identified large nuclear protein assemblies that
can persist for years in post-mitotic tissues and are subject to age-related decline.
Here, we report that mitochondria can be long lived in the mouse brain and reveal
that specific mitochondrial proteins have half-lives longer than the average proteome.
These mitochondrial long-lived proteins (mitoLLPs) are core components of the
electron transport chain (ETC) and display increased longevity in respiratory
supercomplexes. We find that COX7C, a mitoLLP that forms a stable contact site
between complexes I and IV, is required for complex IV and supercomplex assembly.
Remarkably, even upon depletion of COX7C transcripts, ETC function is maintained
for days, effectively uncoupling mitochondrial function from ongoing transcription
of its mitoLLPs. Our results suggest that modulating protein longevity within
the ETC is critical for mitochondrial proteome maintenance and the robustness
of mitochondrial function.
article_processing_charge: No
article_type: original
author:
- first_name: Shefali
full_name: Krishna, Shefali
last_name: Krishna
- first_name: Rafael
full_name: Arrojo e Drigo, Rafael
last_name: Arrojo e Drigo
- first_name: Juliana S.
full_name: Capitanio, Juliana S.
last_name: Capitanio
- first_name: Ranjan
full_name: Ramachandra, Ranjan
last_name: Ramachandra
- first_name: Mark
full_name: Ellisman, Mark
last_name: Ellisman
- 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: Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer
M. Identification of long-lived proteins in the mitochondria reveals increased
stability of the electron transport chain. Developmental Cell. 2021;56(21):P2952-2965.e9.
doi:10.1016/j.devcel.2021.10.008
apa: Krishna, S., Arrojo e Drigo, R., Capitanio, J. S., Ramachandra, R., Ellisman,
M., & Hetzer, M. (2021). Identification of long-lived proteins in the mitochondria
reveals increased stability of the electron transport chain. Developmental
Cell. Elsevier. https://doi.org/10.1016/j.devcel.2021.10.008
chicago: Krishna, Shefali, Rafael Arrojo e Drigo, Juliana S. Capitanio, Ranjan Ramachandra,
Mark Ellisman, and Martin Hetzer. “Identification of Long-Lived Proteins in the
Mitochondria Reveals Increased Stability of the Electron Transport Chain.” Developmental
Cell. Elsevier, 2021. https://doi.org/10.1016/j.devcel.2021.10.008.
ieee: S. Krishna, R. Arrojo e Drigo, J. S. Capitanio, R. Ramachandra, M. Ellisman,
and M. Hetzer, “Identification of long-lived proteins in the mitochondria reveals
increased stability of the electron transport chain,” Developmental Cell,
vol. 56, no. 21. Elsevier, p. P2952–2965.e9, 2021.
ista: Krishna S, Arrojo e Drigo R, Capitanio JS, Ramachandra R, Ellisman M, Hetzer
M. 2021. Identification of long-lived proteins in the mitochondria reveals increased
stability of the electron transport chain. Developmental Cell. 56(21), P2952–2965.e9.
mla: Krishna, Shefali, et al. “Identification of Long-Lived Proteins in the Mitochondria
Reveals Increased Stability of the Electron Transport Chain.” Developmental
Cell, vol. 56, no. 21, Elsevier, 2021, p. P2952–2965.e9, doi:10.1016/j.devcel.2021.10.008.
short: S. Krishna, R. Arrojo e Drigo, J.S. Capitanio, R. Ramachandra, M. Ellisman,
M. Hetzer, Developmental Cell 56 (2021) P2952–2965.e9.
date_created: 2022-04-07T07:43:14Z
date_published: 2021-11-08T00:00:00Z
date_updated: 2022-07-18T08:26:38Z
day: '08'
doi: 10.1016/j.devcel.2021.10.008
extern: '1'
external_id:
pmid:
- '34715012'
intvolume: ' 56'
issue: '21'
keyword:
- Developmental Biology
- Cell Biology
- General Biochemistry
- Genetics and Molecular Biology
- Molecular Biology
language:
- iso: eng
month: '11'
oa_version: None
page: P2952-2965.e9
pmid: 1
publication: Developmental Cell
publication_identifier:
issn:
- 1534-5807
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Identification of long-lived proteins in the mitochondria reveals increased
stability of the electron transport chain
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 56
year: '2021'
...
---
_id: '13356'
abstract:
- lang: eng
text: 'Self-assembly of nanoparticles can be mediated by polymers, but has so far
led almost exclusively to nanoparticle aggregates that are amorphous. Here, we
employed Coulombic interactions to generate a range of composite materials from
mixtures of charged nanoparticles and oppositely charged polymers. The assembly
behavior of these nanoparticle/polymer composites depends on their order of addition:
polymers added to nanoparticles give rise to stable aggregates, but nanoparticles
added to polymers disassemble the initially formed aggregates. The amorphous aggregates
were transformed into crystalline ones by transiently increasing the ionic strength
of the solution. The morphology of the resulting crystals depended on the length
of the polymer: short polymer chains mediated the self-assembly of nanoparticles
into strongly faceted crystals, whereas long chains led to pseudospherical nanoparticle/polymer
assemblies, within which the crystalline order of nanoparticles was retained.'
article_processing_charge: No
article_type: original
author:
- first_name: Tong
full_name: Bian, Tong
last_name: Bian
- first_name: Rafal
full_name: Klajn, Rafal
id: 8e84690e-1e48-11ed-a02b-a1e6fb8bb53b
last_name: Klajn
citation:
ama: Bian T, Klajn R. Morphology control in crystalline nanoparticle–polymer aggregates.
Annals of the New York Academy of Sciences. 2021;1505(1):191-201. doi:10.1111/nyas.14674
apa: Bian, T., & Klajn, R. (2021). Morphology control in crystalline nanoparticle–polymer
aggregates. Annals of the New York Academy of Sciences. Wiley. https://doi.org/10.1111/nyas.14674
chicago: Bian, Tong, and Rafal Klajn. “Morphology Control in Crystalline Nanoparticle–Polymer
Aggregates.” Annals of the New York Academy of Sciences. Wiley, 2021. https://doi.org/10.1111/nyas.14674.
ieee: T. Bian and R. Klajn, “Morphology control in crystalline nanoparticle–polymer
aggregates,” Annals of the New York Academy of Sciences, vol. 1505, no.
1. Wiley, pp. 191–201, 2021.
ista: Bian T, Klajn R. 2021. Morphology control in crystalline nanoparticle–polymer
aggregates. Annals of the New York Academy of Sciences. 1505(1), 191–201.
mla: Bian, Tong, and Rafal Klajn. “Morphology Control in Crystalline Nanoparticle–Polymer
Aggregates.” Annals of the New York Academy of Sciences, vol. 1505, no.
1, Wiley, 2021, pp. 191–201, doi:10.1111/nyas.14674.
short: T. Bian, R. Klajn, Annals of the New York Academy of Sciences 1505 (2021)
191–201.
date_created: 2023-08-01T09:33:39Z
date_published: 2021-12-01T00:00:00Z
date_updated: 2023-08-07T10:01:10Z
day: '01'
ddc:
- '540'
doi: 10.1111/nyas.14674
extern: '1'
external_id:
pmid:
- '34427923'
intvolume: ' 1505'
issue: '1'
keyword:
- History and Philosophy of Science
- General Biochemistry
- Genetics and Molecular Biology
- General Neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1111/nyas.14674
month: '12'
oa: 1
oa_version: Published Version
page: 191-201
pmid: 1
publication: Annals of the New York Academy of Sciences
publication_identifier:
eissn:
- 1749-6632
issn:
- 0077-8923
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Morphology control in crystalline nanoparticle–polymer aggregates
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1505
year: '2021'
...
---
_id: '13359'
abstract:
- lang: eng
text: Dissipative self-assembly is ubiquitous in nature, where it gives rise to
complex structures and functions such as self-healing, homeostasis, and camouflage.
These phenomena are enabled by the continuous conversion of energy stored in chemical
fuels, such as ATP. Over the past decade, an increasing number of synthetic chemically
driven systems have been reported that mimic the features of their natural counterparts.
At the same time, it has been shown that dissipative self-assembly can also be
fueled by light; these optically fueled systems have been developed in parallel
to the chemically fueled ones. In this perspective, we critically compare these
two classes of systems. Despite the complementarity and fundamental differences
between these two modes of dissipative self-assembly, our analysis reveals that
multiple analogies exist between chemically and light-fueled systems. We hope
that these considerations will facilitate further development of the field of
dissipative self-assembly.
article_processing_charge: No
article_type: original
author:
- first_name: Maren
full_name: Weißenfels, Maren
last_name: Weißenfels
- first_name: Julius
full_name: Gemen, Julius
last_name: Gemen
- first_name: Rafal
full_name: Klajn, Rafal
id: 8e84690e-1e48-11ed-a02b-a1e6fb8bb53b
last_name: Klajn
citation:
ama: 'Weißenfels M, Gemen J, Klajn R. Dissipative self-assembly: Fueling with chemicals
versus light. Chem. 2021;7(1):23-37. doi:10.1016/j.chempr.2020.11.025'
apa: 'Weißenfels, M., Gemen, J., & Klajn, R. (2021). Dissipative self-assembly:
Fueling with chemicals versus light. Chem. Elsevier. https://doi.org/10.1016/j.chempr.2020.11.025'
chicago: 'Weißenfels, Maren, Julius Gemen, and Rafal Klajn. “Dissipative Self-Assembly:
Fueling with Chemicals versus Light.” Chem. Elsevier, 2021. https://doi.org/10.1016/j.chempr.2020.11.025.'
ieee: 'M. Weißenfels, J. Gemen, and R. Klajn, “Dissipative self-assembly: Fueling
with chemicals versus light,” Chem, vol. 7, no. 1. Elsevier, pp. 23–37,
2021.'
ista: 'Weißenfels M, Gemen J, Klajn R. 2021. Dissipative self-assembly: Fueling
with chemicals versus light. Chem. 7(1), 23–37.'
mla: 'Weißenfels, Maren, et al. “Dissipative Self-Assembly: Fueling with Chemicals
versus Light.” Chem, vol. 7, no. 1, Elsevier, 2021, pp. 23–37, doi:10.1016/j.chempr.2020.11.025.'
short: M. Weißenfels, J. Gemen, R. Klajn, Chem 7 (2021) 23–37.
date_created: 2023-08-01T09:35:19Z
date_published: 2021-01-14T00:00:00Z
date_updated: 2023-08-07T10:04:28Z
day: '14'
doi: 10.1016/j.chempr.2020.11.025
extern: '1'
intvolume: ' 7'
issue: '1'
keyword:
- Materials Chemistry
- Biochemistry (medical)
- General Chemical Engineering
- Environmental Chemistry
- Biochemistry
- General Chemistry
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.chempr.2020.11.025
month: '01'
oa: 1
oa_version: Published Version
page: 23-37
publication: Chem
publication_identifier:
issn:
- 2451-9294
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Dissipative self-assembly: Fueling with chemicals versus light'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 7
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: '9429'
abstract:
- lang: eng
text: De novo loss of function mutations in the ubiquitin ligase-encoding gene Cullin3
lead to autism spectrum disorder (ASD). In mouse, constitutive haploinsufficiency
leads to motor coordination deficits as well as ASD-relevant social and cognitive
impairments. However, induction of Cul3 haploinsufficiency later in life does
not lead to ASD-relevant behaviors, pointing to an important role of Cul3 during
a critical developmental window. Here we show that Cul3 is essential to regulate
neuronal migration and, therefore, constitutive Cul3 heterozygous mutant mice
display cortical lamination abnormalities. At the molecular level, we found that
Cul3 controls neuronal migration by tightly regulating the amount of Plastin3
(Pls3), a previously unrecognized player of neural migration. Furthermore, we
found that Pls3 cell-autonomously regulates cell migration by regulating actin
cytoskeleton organization, and its levels are inversely proportional to neural
migration speed. Finally, we provide evidence that cellular phenotypes associated
with autism-linked gene haploinsufficiency can be rescued by transcriptional activation
of the intact allele in vitro, offering a proof of concept for a potential therapeutic
approach for ASDs.
acknowledged_ssus:
- _id: PreCl
acknowledgement: We thank A. Coll Manzano, F. Freeman, M. Ladron de Guevara, and A.
Ç. Yahya for technical assistance, S. Deixler, A. Lepold, and A. Schlerka for the
management of our animal colony, as well as M. Schunn and the Preclinical Facility
team for technical assistance. We thank K. Heesom and her team at the University
of Bristol Proteomics Facility for the proteomics sample preparation, data generation,
and analysis support. We thank Y. B. Simon for kindly providing the plasmid for
lentiviral labeling. Further, we thank M. Sixt for his advice regarding cell migration
and the fruitful discussions. This work was supported by the ISTPlus postdoctoral
fellowship (Grant Agreement No. 754411) to B.B., by the European Union’s Horizon
2020 research and innovation program (ERC) grant 715508 (REVERSEAUTISM), and by
the Austrian Science Fund (FWF) to G.N. (DK W1232-B24 and SFB F7807-B) and to J.G.D
(I3600-B27).
article_number: '3058'
article_processing_charge: No
article_type: original
author:
- first_name: Jasmin
full_name: Morandell, Jasmin
id: 4739D480-F248-11E8-B48F-1D18A9856A87
last_name: Morandell
- first_name: Lena A
full_name: Schwarz, Lena A
id: 29A8453C-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Bernadette
full_name: Basilico, Bernadette
id: 36035796-5ACA-11E9-A75E-7AF2E5697425
last_name: Basilico
orcid: 0000-0003-1843-3173
- first_name: Saren
full_name: Tasciyan, Saren
id: 4323B49C-F248-11E8-B48F-1D18A9856A87
last_name: Tasciyan
orcid: 0000-0003-1671-393X
- first_name: Georgi A
full_name: Dimchev, Georgi A
id: 38C393BE-F248-11E8-B48F-1D18A9856A87
last_name: Dimchev
orcid: 0000-0001-8370-6161
- first_name: Armel
full_name: Nicolas, Armel
id: 2A103192-F248-11E8-B48F-1D18A9856A87
last_name: Nicolas
- first_name: Christoph M
full_name: Sommer, Christoph M
id: 4DF26D8C-F248-11E8-B48F-1D18A9856A87
last_name: Sommer
orcid: 0000-0003-1216-9105
- first_name: Caroline
full_name: Kreuzinger, Caroline
id: 382077BA-F248-11E8-B48F-1D18A9856A87
last_name: Kreuzinger
- first_name: Christoph
full_name: Dotter, Christoph
id: 4C66542E-F248-11E8-B48F-1D18A9856A87
last_name: Dotter
orcid: 0000-0002-9033-9096
- first_name: Lisa
full_name: Knaus, Lisa
id: 3B2ABCF4-F248-11E8-B48F-1D18A9856A87
last_name: Knaus
- first_name: Zoe
full_name: Dobler, Zoe
id: D23090A2-9057-11EA-883A-A8396FC7A38F
last_name: Dobler
- first_name: Emanuele
full_name: Cacci, Emanuele
last_name: Cacci
- 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: Johann G
full_name: Danzl, Johann G
id: 42EFD3B6-F248-11E8-B48F-1D18A9856A87
last_name: Danzl
orcid: 0000-0001-8559-3973
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
citation:
ama: Morandell J, Schwarz LA, Basilico B, et al. Cul3 regulates cytoskeleton protein
homeostasis and cell migration during a critical window of brain development.
Nature Communications. 2021;12(1). doi:10.1038/s41467-021-23123-x
apa: Morandell, J., Schwarz, L. A., Basilico, B., Tasciyan, S., Dimchev, G. A.,
Nicolas, A., … Novarino, G. (2021). Cul3 regulates cytoskeleton protein homeostasis
and cell migration during a critical window of brain development. Nature Communications.
Springer Nature. https://doi.org/10.1038/s41467-021-23123-x
chicago: Morandell, Jasmin, Lena A Schwarz, Bernadette Basilico, Saren Tasciyan,
Georgi A Dimchev, Armel Nicolas, Christoph M Sommer, et al. “Cul3 Regulates Cytoskeleton
Protein Homeostasis and Cell Migration during a Critical Window of Brain Development.”
Nature Communications. Springer Nature, 2021. https://doi.org/10.1038/s41467-021-23123-x.
ieee: J. Morandell et al., “Cul3 regulates cytoskeleton protein homeostasis
and cell migration during a critical window of brain development,” Nature Communications,
vol. 12, no. 1. Springer Nature, 2021.
ista: Morandell J, Schwarz LA, Basilico B, Tasciyan S, Dimchev GA, Nicolas A, Sommer
CM, Kreuzinger C, Dotter C, Knaus L, Dobler Z, Cacci E, Schur FK, Danzl JG, Novarino
G. 2021. Cul3 regulates cytoskeleton protein homeostasis and cell migration during
a critical window of brain development. Nature Communications. 12(1), 3058.
mla: Morandell, Jasmin, et al. “Cul3 Regulates Cytoskeleton Protein Homeostasis
and Cell Migration during a Critical Window of Brain Development.” Nature Communications,
vol. 12, no. 1, 3058, Springer Nature, 2021, doi:10.1038/s41467-021-23123-x.
short: J. Morandell, L.A. Schwarz, B. Basilico, S. Tasciyan, G.A. Dimchev, A. Nicolas,
C.M. Sommer, C. Kreuzinger, C. Dotter, L. Knaus, Z. Dobler, E. Cacci, F.K. Schur,
J.G. Danzl, G. Novarino, Nature Communications 12 (2021).
date_created: 2021-05-28T11:49:46Z
date_published: 2021-05-24T00:00:00Z
date_updated: 2024-09-10T12:04:26Z
day: '24'
ddc:
- '572'
department:
- _id: GaNo
- _id: JoDa
- _id: FlSc
- _id: MiSi
- _id: LifeSc
- _id: Bio
doi: 10.1038/s41467-021-23123-x
ec_funded: 1
external_id:
isi:
- '000658769900010'
file:
- access_level: open_access
checksum: 337e0f7959c35ec959984cacdcb472ba
content_type: application/pdf
creator: kschuh
date_created: 2021-05-28T12:39:43Z
date_updated: 2021-05-28T12:39:43Z
file_id: '9430'
file_name: 2021_NatureCommunications_Morandell.pdf
file_size: 9358599
relation: main_file
success: 1
file_date_updated: 2021-05-28T12:39:43Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
issue: '1'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 25444568-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '715508'
name: Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo
and in vitro Models
- _id: 2548AE96-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W1232-B24
name: Molecular Drug Targets
- _id: 05A0D778-7A3F-11EA-A408-12923DDC885E
grant_number: F07807
name: Neural stem cells in autism and epilepsy
- _id: 265CB4D0-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I03600
name: Optical control of synaptic function via adhesion molecules
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: press_release
url: https://ist.ac.at/en/news/defective-gene-slows-down-brain-cells/
record:
- id: '7800'
relation: earlier_version
status: public
- id: '12401'
relation: dissertation_contains
status: public
status: public
title: Cul3 regulates cytoskeleton protein homeostasis and cell migration during a
critical window of brain development
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: 12
year: '2021'
...
---
_id: '9431'
abstract:
- lang: eng
text: Inositol hexakisphosphate (IP6) is an assembly cofactor for HIV-1. We report
here that IP6 is also used for assembly of Rous sarcoma virus (RSV), a retrovirus
from a different genus. IP6 is ~100-fold more potent at promoting RSV mature capsid
protein (CA) assembly than observed for HIV-1 and removal of IP6 in cells reduces
infectivity by 100-fold. Here, visualized by cryo-electron tomography and subtomogram
averaging, mature capsid-like particles show an IP6-like density in the CA hexamer,
coordinated by rings of six lysines and six arginines. Phosphate and IP6 have
opposing effects on CA in vitro assembly, inducing formation of T = 1 icosahedrons
and tubes, respectively, implying that phosphate promotes pentamer and IP6 hexamer
formation. Subtomogram averaging and classification optimized for analysis of
pleomorphic retrovirus particles reveal that the heterogeneity of mature RSV CA
polyhedrons results from an unexpected, intrinsic CA hexamer flexibility. In contrast,
the CA pentamer forms rigid units organizing the local architecture. These different
features of hexamers and pentamers determine the structural mechanism to form
CA polyhedrons of variable shape in mature RSV particles.
acknowledged_ssus:
- _id: ScienComp
- _id: LifeSc
- _id: EM-Fac
acknowledgement: This work was funded by the National Institute of Allergy and Infectious
Diseases under awards R01AI147890 to R.A.D., R01AI150454 to V.M.V, R35GM136258 in
support of J-P.R.F, and the Austrian Science Fund (FWF) grant P31445 to F.K.M.S.
Access to high-resolution cryo-ET data acquisition at EMBL Heidelberg was supported
by iNEXT (grant no. 653706), funded by the Horizon 2020 program of the European
Union (PID 4246). We thank Wim Hagen and Felix Weis at EMBL Heidelberg for support
in cryo-ET data acquisition. This work made use of the Cornell Center for Materials
Research Shared Facilities, which are supported through the NSF MRSEC program (DMR-179875).
This research was also supported by the Scientific Service Units (SSUs) of IST Austria
through resources provided by Scientific Computing (SciComp), the Life Science Facility
(LSF), and the Electron Microscopy Facility (EMF).
article_number: '3226'
article_processing_charge: No
article_type: original
author:
- first_name: Martin
full_name: Obr, Martin
id: 4741CA5A-F248-11E8-B48F-1D18A9856A87
last_name: Obr
- first_name: Clifton L.
full_name: Ricana, Clifton L.
last_name: Ricana
- first_name: Nadia
full_name: Nikulin, Nadia
last_name: Nikulin
- first_name: Jon-Philip R.
full_name: Feathers, Jon-Philip R.
last_name: Feathers
- first_name: Marco
full_name: Klanschnig, Marco
last_name: Klanschnig
- first_name: Andreas
full_name: Thader, Andreas
id: 3A18A7B8-F248-11E8-B48F-1D18A9856A87
last_name: Thader
- first_name: Marc C.
full_name: Johnson, Marc C.
last_name: Johnson
- first_name: Volker M.
full_name: Vogt, Volker M.
last_name: Vogt
- 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: Robert A.
full_name: Dick, Robert A.
last_name: Dick
citation:
ama: Obr M, Ricana CL, Nikulin N, et al. Structure of the mature Rous sarcoma virus
lattice reveals a role for IP6 in the formation of the capsid hexamer. Nature
Communications. 2021;12(1). doi:10.1038/s41467-021-23506-0
apa: Obr, M., Ricana, C. L., Nikulin, N., Feathers, J.-P. R., Klanschnig, M., Thader,
A., … Dick, R. A. (2021). Structure of the mature Rous sarcoma virus lattice reveals
a role for IP6 in the formation of the capsid hexamer. Nature Communications.
Nature Research. https://doi.org/10.1038/s41467-021-23506-0
chicago: Obr, Martin, Clifton L. Ricana, Nadia Nikulin, Jon-Philip R. Feathers,
Marco Klanschnig, Andreas Thader, Marc C. Johnson, Volker M. Vogt, Florian KM
Schur, and Robert A. Dick. “Structure of the Mature Rous Sarcoma Virus Lattice
Reveals a Role for IP6 in the Formation of the Capsid Hexamer.” Nature Communications.
Nature Research, 2021. https://doi.org/10.1038/s41467-021-23506-0.
ieee: M. Obr et al., “Structure of the mature Rous sarcoma virus lattice
reveals a role for IP6 in the formation of the capsid hexamer,” Nature Communications,
vol. 12, no. 1. Nature Research, 2021.
ista: Obr M, Ricana CL, Nikulin N, Feathers J-PR, Klanschnig M, Thader A, Johnson
MC, Vogt VM, Schur FK, Dick RA. 2021. Structure of the mature Rous sarcoma virus
lattice reveals a role for IP6 in the formation of the capsid hexamer. Nature
Communications. 12(1), 3226.
mla: Obr, Martin, et al. “Structure of the Mature Rous Sarcoma Virus Lattice Reveals
a Role for IP6 in the Formation of the Capsid Hexamer.” Nature Communications,
vol. 12, no. 1, 3226, Nature Research, 2021, doi:10.1038/s41467-021-23506-0.
short: M. Obr, C.L. Ricana, N. Nikulin, J.-P.R. Feathers, M. Klanschnig, A. Thader,
M.C. Johnson, V.M. Vogt, F.K. Schur, R.A. Dick, Nature Communications 12 (2021).
date_created: 2021-05-28T14:25:50Z
date_published: 2021-05-28T00:00:00Z
date_updated: 2023-08-08T13:53:53Z
day: '28'
ddc:
- '570'
department:
- _id: FlSc
doi: 10.1038/s41467-021-23506-0
external_id:
isi:
- '000659145000011'
file:
- access_level: open_access
checksum: 53ccc53d09a9111143839dbe7784e663
content_type: application/pdf
creator: kschuh
date_created: 2021-06-09T15:21:14Z
date_updated: 2021-06-09T15:21:14Z
file_id: '9538'
file_name: 2021_NatureCommunications_Obr.pdf
file_size: 6166295
relation: main_file
success: 1
file_date_updated: 2021-06-09T15:21:14Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
issue: '1'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- General Physics and Astronomy
- General Chemistry
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 26736D6A-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P31445
name: Structural conservation and diversity in retroviral capsid
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Nature Research
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/how-retroviruses-become-infectious/
scopus_import: '1'
status: public
title: Structure of the mature Rous sarcoma virus lattice reveals a role for IP6 in
the formation of the capsid hexamer
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: 12
year: '2021'
...
---
_id: '9540'
abstract:
- lang: eng
text: The hexameric AAA-ATPase Drg1 is a key factor in eukaryotic ribosome biogenesis
and initiates cytoplasmic maturation of the large ribosomal subunit by releasing
the shuttling maturation factor Rlp24. Drg1 monomers contain two AAA-domains (D1
and D2) that act in a concerted manner. Rlp24 release is inhibited by the drug
diazaborine which blocks ATP hydrolysis in D2. The mode of inhibition was unknown.
Here we show the first cryo-EM structure of Drg1 revealing the inhibitory mechanism.
Diazaborine forms a covalent bond to the 2′-OH of the nucleotide in D2, explaining
its specificity for this site. As a consequence, the D2 domain is locked in a
rigid, inactive state, stalling the whole Drg1 hexamer. Resistance mechanisms
identified include abolished drug binding and altered positioning of the nucleotide.
Our results suggest nucleotide-modifying compounds as potential novel inhibitors
for AAA-ATPases.
acknowledged_ssus:
- _id: EM-Fac
acknowledgement: We are deeply grateful to the late Gregor Högenauer who built the
foundation for this study with his visionary work on the inhibitor diazaborine and
its bacterial target. We thank Rolf Breinbauer for insightful discussions on boron
chemistry. We thank Anton Meinhart and Tim Clausen for the valuable discussion of
the manuscript. We are indebted to Thomas Köcher for the MS measurement of the diazaborine-ATPγS
adduct. We thank the team of the VBCF for support during early phases of this work
and the IST Austria Electron Microscopy Facility for providing equipment. The lab
of D.H. is supported by Boehringer Ingelheim. The work was funded by FWF projects
P32536 and P32977 (to H.B.).
article_number: '3483'
article_processing_charge: No
article_type: original
author:
- first_name: Michael
full_name: Prattes, Michael
last_name: Prattes
- first_name: Irina
full_name: Grishkovskaya, Irina
last_name: Grishkovskaya
- first_name: Victor-Valentin
full_name: Hodirnau, Victor-Valentin
id: 3661B498-F248-11E8-B48F-1D18A9856A87
last_name: Hodirnau
- first_name: Ingrid
full_name: Rössler, Ingrid
last_name: Rössler
- first_name: Isabella
full_name: Klein, Isabella
last_name: Klein
- first_name: Christina
full_name: Hetzmannseder, Christina
last_name: Hetzmannseder
- first_name: Gertrude
full_name: Zisser, Gertrude
last_name: Zisser
- first_name: Christian C.
full_name: Gruber, Christian C.
last_name: Gruber
- first_name: Karl
full_name: Gruber, Karl
last_name: Gruber
- first_name: David
full_name: Haselbach, David
last_name: Haselbach
- first_name: Helmut
full_name: Bergler, Helmut
last_name: Bergler
citation:
ama: Prattes M, Grishkovskaya I, Hodirnau V-V, et al. Structural basis for inhibition
of the AAA-ATPase Drg1 by diazaborine. Nature Communications. 2021;12(1).
doi:10.1038/s41467-021-23854-x
apa: Prattes, M., Grishkovskaya, I., Hodirnau, V.-V., Rössler, I., Klein, I., Hetzmannseder,
C., … Bergler, H. (2021). Structural basis for inhibition of the AAA-ATPase Drg1
by diazaborine. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-021-23854-x
chicago: Prattes, Michael, Irina Grishkovskaya, Victor-Valentin Hodirnau, Ingrid
Rössler, Isabella Klein, Christina Hetzmannseder, Gertrude Zisser, et al. “Structural
Basis for Inhibition of the AAA-ATPase Drg1 by Diazaborine.” Nature Communications.
Springer Nature, 2021. https://doi.org/10.1038/s41467-021-23854-x.
ieee: M. Prattes et al., “Structural basis for inhibition of the AAA-ATPase
Drg1 by diazaborine,” Nature Communications, vol. 12, no. 1. Springer Nature,
2021.
ista: Prattes M, Grishkovskaya I, Hodirnau V-V, Rössler I, Klein I, Hetzmannseder
C, Zisser G, Gruber CC, Gruber K, Haselbach D, Bergler H. 2021. Structural basis
for inhibition of the AAA-ATPase Drg1 by diazaborine. Nature Communications. 12(1),
3483.
mla: Prattes, Michael, et al. “Structural Basis for Inhibition of the AAA-ATPase
Drg1 by Diazaborine.” Nature Communications, vol. 12, no. 1, 3483, Springer
Nature, 2021, doi:10.1038/s41467-021-23854-x.
short: M. Prattes, I. Grishkovskaya, V.-V. Hodirnau, I. Rössler, I. Klein, C. Hetzmannseder,
G. Zisser, C.C. Gruber, K. Gruber, D. Haselbach, H. Bergler, Nature Communications
12 (2021).
date_created: 2021-06-10T14:57:45Z
date_published: 2021-06-09T00:00:00Z
date_updated: 2023-08-08T14:05:26Z
day: '09'
ddc:
- '570'
department:
- _id: EM-Fac
doi: 10.1038/s41467-021-23854-x
external_id:
isi:
- '000664874700014'
pmid:
- '34108481'
file:
- access_level: open_access
checksum: 40fc24c1310930990b52a8ad1142ee97
content_type: application/pdf
creator: cziletti
date_created: 2021-06-15T18:55:59Z
date_updated: 2021-06-15T18:55:59Z
file_id: '9556'
file_name: 2021_NatureComm_Prattes.pdf
file_size: 3397292
relation: main_file
success: 1
file_date_updated: 2021-06-15T18:55:59Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
issue: '1'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- General Physics and Astronomy
- General Chemistry
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Structural basis for inhibition of the AAA-ATPase Drg1 by diazaborine
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: 12
year: '2021'
...
---
_id: '10163'
abstract:
- lang: eng
text: The C-terminal domain (CTD) of the largest subunit of RNA polymerase II (Pol
II) is a regulatory hub for transcription and RNA processing. Here, we identify
PHD-finger protein 3 (PHF3) as a regulator of transcription and mRNA stability
that docks onto Pol II CTD through its SPOC domain. We characterize SPOC as a
CTD reader domain that preferentially binds two phosphorylated Serine-2 marks
in adjacent CTD repeats. PHF3 drives liquid-liquid phase separation of phosphorylated
Pol II, colocalizes with Pol II clusters and tracks with Pol II across the length
of genes. PHF3 knock-out or SPOC deletion in human cells results in increased
Pol II stalling, reduced elongation rate and an increase in mRNA stability, with
marked derepression of neuronal genes. Key neuronal genes are aberrantly expressed
in Phf3 knock-out mouse embryonic stem cells, resulting in impaired neuronal differentiation.
Our data suggest that PHF3 acts as a prominent effector of neuronal gene regulation
by bridging transcription with mRNA decay.
acknowledgement: 'D.S. thanks Claudine Kraft, Renée Schroeder, Verena Jantsch, Franz
Klein and Peter Schlögelhofer for support. We thank Anita Testa Salmazo for help
with purifying Pol II; Matthias Geyer and Robert Düster for sharing DYRK1A kinase;
Felix Hartmann and Clemens Plaschka for help with mass photometry; Goran Kokic for
design of the arrest assay sequences; Petra van der Lelij for help with generating
mESC KO; Maximilian Freilinger for help with the purification of mEGFP-CTD; Stefan
Ameres, Nina Fasching and Brian Reichholf for advice on SLAM-seq and for sharing
reagents; Laura Gallego Valle for advice regarding LLPS assays; Krzysztof Chylinski
for advice regarding CRISPR/Cas9 methodology; VBCF Protein Technologies facility
for purifying PHF3 and providing gRNAs and Cas9; VBCF NGS facility for sequencing;
Monoclonal antibody facility at the Helmholtz center for Pol II antibodies; Friedrich
Propst and Elzbieta Kowalska for advice and for sharing materials; Egon Ogris for
sharing materials; Martin Eilers for recommending a ChIP-grade TFIIS antibody; Susanne
Opravil, Otto Hudecz, Markus Hartl and Natascha Hartl for mass spectrometry analysis;
staff of the X-ray beamlines at the ESRF in Grenoble for their excellent support;
Christa Bücker, Anton Meinhart, Clemens Plaschka and members of the Slade lab for
critical comments on the manuscript; Life Science Editors for editing assistance.
M.B. and D.S. acknowledge support by the FWF-funded DK ‘Chromosome Dynamics’. T.K.
is a recipient of the DOC fellowship from the Austrian Academy of Sciences. U.S.
is supported by the L’Oreal for Women in Science Austria Fellowship and the Austrian
Science Fund (FWF T 795-B30). M.L is supported by the Vienna Science and Technology
Fund (WWTF, VRG14-006). R.S. is supported by the Czech Science Foundation (15-17670 S
and 21-24460 S), Ministry of Education, Youths and Sports of the Czech Republic
(CEITEC 2020 project (LQ1601)), and the European Research Council (ERC) under the
European Union’s Horizon 2020 research and innovation programme (Grant agreement
no. 649030); this publication reflects only the author’s view and the Research Executive
Agency is not responsible for any use that may be made of the information it contains.
M.S. is supported by the Czech Science Foundation (GJ20-21581Y). K.D.C. research
is supported by the Austrian Science Fund (FWF) Projects I525 and I1593, P22276,
P19060, and W1221, Federal Ministry of Economy, Family and Youth through the initiative
‘Laura Bassi Centres of Expertise’, funding from the Centre of Optimized Structural
Studies No. 253275, the Wellcome Trust Collaborative Award (201543/Z/16), COST action
BM1405 Non-globular proteins - from sequence to structure, function and application
in molecular physiopathology (NGP-NET), the Vienna Science and Technology Fund (WWTF
LS17-008), and by the University of Vienna. This project was funded by the MFPL
start-up grant, the Vienna Science and Technology Fund (WWTF LS14-001), and the
Austrian Science Fund (P31546-B28 and W1258 “DK: Integrative Structural Biology”)
to D.S.'
article_number: '6078'
article_processing_charge: No
article_type: original
author:
- first_name: Lisa-Marie
full_name: Appel, Lisa-Marie
last_name: Appel
- first_name: Vedran
full_name: Franke, Vedran
last_name: Franke
- first_name: Melania
full_name: Bruno, Melania
last_name: Bruno
- first_name: Irina
full_name: Grishkovskaya, Irina
last_name: Grishkovskaya
- first_name: Aiste
full_name: Kasiliauskaite, Aiste
last_name: Kasiliauskaite
- first_name: Tanja
full_name: Kaufmann, Tanja
last_name: Kaufmann
- first_name: Ursula E.
full_name: Schoeberl, Ursula E.
last_name: Schoeberl
- first_name: Martin G.
full_name: Puchinger, Martin G.
last_name: Puchinger
- first_name: Sebastian
full_name: Kostrhon, Sebastian
last_name: Kostrhon
- first_name: Carmen
full_name: Ebenwaldner, Carmen
last_name: Ebenwaldner
- first_name: Marek
full_name: Sebesta, Marek
last_name: Sebesta
- first_name: Etienne
full_name: Beltzung, Etienne
last_name: Beltzung
- first_name: Karl
full_name: Mechtler, Karl
last_name: Mechtler
- first_name: Gen
full_name: Lin, Gen
last_name: Lin
- first_name: Anna
full_name: Vlasova, Anna
last_name: Vlasova
- first_name: Martin
full_name: Leeb, Martin
last_name: Leeb
- first_name: Rushad
full_name: Pavri, Rushad
last_name: Pavri
- first_name: Alexander
full_name: Stark, Alexander
last_name: Stark
- first_name: Altuna
full_name: Akalin, Altuna
last_name: Akalin
- first_name: Richard
full_name: Stefl, Richard
last_name: Stefl
- first_name: Carrie A
full_name: Bernecky, Carrie A
id: 2CB9DFE2-F248-11E8-B48F-1D18A9856A87
last_name: Bernecky
orcid: 0000-0003-0893-7036
- first_name: Kristina
full_name: Djinovic-Carugo, Kristina
last_name: Djinovic-Carugo
- first_name: Dea
full_name: Slade, Dea
last_name: Slade
citation:
ama: Appel L-M, Franke V, Bruno M, et al. PHF3 regulates neuronal gene expression
through the Pol II CTD reader domain SPOC. Nature Communications. 2021;12(1).
doi:10.1038/s41467-021-26360-2
apa: Appel, L.-M., Franke, V., Bruno, M., Grishkovskaya, I., Kasiliauskaite, A.,
Kaufmann, T., … Slade, D. (2021). PHF3 regulates neuronal gene expression through
the Pol II CTD reader domain SPOC. Nature Communications. Springer Nature.
https://doi.org/10.1038/s41467-021-26360-2
chicago: Appel, Lisa-Marie, Vedran Franke, Melania Bruno, Irina Grishkovskaya, Aiste
Kasiliauskaite, Tanja Kaufmann, Ursula E. Schoeberl, et al. “PHF3 Regulates Neuronal
Gene Expression through the Pol II CTD Reader Domain SPOC.” Nature Communications.
Springer Nature, 2021. https://doi.org/10.1038/s41467-021-26360-2.
ieee: L.-M. Appel et al., “PHF3 regulates neuronal gene expression through
the Pol II CTD reader domain SPOC,” Nature Communications, vol. 12, no.
1. Springer Nature, 2021.
ista: Appel L-M, Franke V, Bruno M, Grishkovskaya I, Kasiliauskaite A, Kaufmann
T, Schoeberl UE, Puchinger MG, Kostrhon S, Ebenwaldner C, Sebesta M, Beltzung
E, Mechtler K, Lin G, Vlasova A, Leeb M, Pavri R, Stark A, Akalin A, Stefl R,
Bernecky C, Djinovic-Carugo K, Slade D. 2021. PHF3 regulates neuronal gene expression
through the Pol II CTD reader domain SPOC. Nature Communications. 12(1), 6078.
mla: Appel, Lisa-Marie, et al. “PHF3 Regulates Neuronal Gene Expression through
the Pol II CTD Reader Domain SPOC.” Nature Communications, vol. 12, no.
1, 6078, Springer Nature, 2021, doi:10.1038/s41467-021-26360-2.
short: L.-M. Appel, V. Franke, M. Bruno, I. Grishkovskaya, A. Kasiliauskaite, T.
Kaufmann, U.E. Schoeberl, M.G. Puchinger, S. Kostrhon, C. Ebenwaldner, M. Sebesta,
E. Beltzung, K. Mechtler, G. Lin, A. Vlasova, M. Leeb, R. Pavri, A. Stark, A.
Akalin, R. Stefl, C. Bernecky, K. Djinovic-Carugo, D. Slade, Nature Communications
12 (2021).
date_created: 2021-10-20T14:40:32Z
date_published: 2021-10-19T00:00:00Z
date_updated: 2023-08-14T08:02:31Z
day: '19'
ddc:
- '610'
department:
- _id: CaBe
doi: 10.1038/s41467-021-26360-2
external_id:
isi:
- '000709050300001'
file:
- access_level: open_access
checksum: d99fcd51aebde19c21314e3de0148007
content_type: application/pdf
creator: cchlebak
date_created: 2021-10-21T13:51:49Z
date_updated: 2021-10-21T13:51:49Z
file_id: '10169'
file_name: 2021_NatComm_Appel.pdf
file_size: 5111706
relation: main_file
success: 1
file_date_updated: 2021-10-21T13:51:49Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
issue: '1'
keyword:
- general physics and astronomy
- general biochemistry
- genetics and molecular biology
- general chemistry
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: 'Preprint '
relation: earlier_version
url: https://www.biorxiv.org/content/10.1101/2020.02.11.943159
status: public
title: PHF3 regulates neuronal gene expression through the Pol II CTD reader domain
SPOC
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: 12
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: '10310'
abstract:
- lang: eng
text: A high-resolution structure of trimeric cyanobacterial Photosystem I (PSI)
from Thermosynechococcus elongatus was reported as the first atomic model of PSI
almost 20 years ago. However, the monomeric PSI structure has not yet been reported
despite long-standing interest in its structure and extensive spectroscopic characterization
of the loss of red chlorophylls upon monomerization. Here, we describe the structure
of monomeric PSI from Thermosynechococcus elongatus BP-1. Comparison with the
trimer structure gave detailed insights into monomerization-induced changes in
both the central trimerization domain and the peripheral regions of the complex.
Monomerization-induced loss of red chlorophylls is assigned to a cluster of chlorophylls
adjacent to PsaX. Based on our findings, we propose a role of PsaX in the stabilization
of red chlorophylls and that lipids of the surrounding membrane present a major
source of thermal energy for uphill excitation energy transfer from red chlorophylls
to P700.
acknowledgement: We are grateful for additional support and valuable scientific input
for this project by Yuko Misumi, Jiannan Li, Hisako Kubota-Kawai, Takeshi Kawabata,
Mian Wu, Eiki Yamashita, Atsushi Nakagawa, Volker Hartmann, Melanie Völkel and Matthias
Rögner. Parts of this research were funded by the German Research Council (DFG)
within the framework of GRK 2341 (Microbial Substrate Conversion) to M.M.N., the
Platform Project for Supporting Drug Discovery and Life Science Research [Basis
for Supporting Innovative Drug Discovery and Life Science Research (BINDS)] from
AMED under grant number JP20am0101117 (K.N.), JP16K07266 to Atsunori Oshima and
C.G., a Grants-in-Aid for Scientific Research under grant number JP 25000013 (K.N.),
17H03647 (C.G.) and 16H06560 (G.K.) from MEXT-KAKENHI, the International Joint Research
Promotion Program from Osaka University to M.M.N., C.G. and G.K., and the Cyclic
Innovation for Clinical Empowerment (CiCLE) Grant Number JP17pc0101020 from AMED
to K.N. and G.K.
article_number: '304'
article_processing_charge: No
article_type: original
author:
- first_name: Mehmet Orkun
full_name: Çoruh, Mehmet Orkun
id: d25163e5-8d53-11eb-a251-e6dd8ea1b8ef
last_name: Çoruh
orcid: 0000-0002-3219-2022
- first_name: Anna
full_name: Frank, Anna
last_name: Frank
- first_name: Hideaki
full_name: Tanaka, Hideaki
last_name: Tanaka
- first_name: Akihiro
full_name: Kawamoto, Akihiro
last_name: Kawamoto
- first_name: Eithar
full_name: El-Mohsnawy, Eithar
last_name: El-Mohsnawy
- first_name: Takayuki
full_name: Kato, Takayuki
last_name: Kato
- first_name: Keiichi
full_name: Namba, Keiichi
last_name: Namba
- first_name: Christoph
full_name: Gerle, Christoph
last_name: Gerle
- first_name: Marc M.
full_name: Nowaczyk, Marc M.
last_name: Nowaczyk
- first_name: Genji
full_name: Kurisu, Genji
last_name: Kurisu
citation:
ama: Çoruh MO, Frank A, Tanaka H, et al. Cryo-EM structure of a functional monomeric
Photosystem I from Thermosynechococcus elongatus reveals red chlorophyll cluster.
Communications Biology. 2021;4(1). doi:10.1038/s42003-021-01808-9
apa: Çoruh, M. O., Frank, A., Tanaka, H., Kawamoto, A., El-Mohsnawy, E., Kato, T.,
… Kurisu, G. (2021). Cryo-EM structure of a functional monomeric Photosystem I
from Thermosynechococcus elongatus reveals red chlorophyll cluster. Communications
Biology. Springer . https://doi.org/10.1038/s42003-021-01808-9
chicago: Çoruh, Mehmet Orkun, Anna Frank, Hideaki Tanaka, Akihiro Kawamoto, Eithar
El-Mohsnawy, Takayuki Kato, Keiichi Namba, Christoph Gerle, Marc M. Nowaczyk,
and Genji Kurisu. “Cryo-EM Structure of a Functional Monomeric Photosystem I from
Thermosynechococcus Elongatus Reveals Red Chlorophyll Cluster.” Communications
Biology. Springer , 2021. https://doi.org/10.1038/s42003-021-01808-9.
ieee: M. O. Çoruh et al., “Cryo-EM structure of a functional monomeric Photosystem
I from Thermosynechococcus elongatus reveals red chlorophyll cluster,” Communications
Biology, vol. 4, no. 1. Springer , 2021.
ista: Çoruh MO, Frank A, Tanaka H, Kawamoto A, El-Mohsnawy E, Kato T, Namba K, Gerle
C, Nowaczyk MM, Kurisu G. 2021. Cryo-EM structure of a functional monomeric Photosystem
I from Thermosynechococcus elongatus reveals red chlorophyll cluster. Communications
Biology. 4(1), 304.
mla: Çoruh, Mehmet Orkun, et al. “Cryo-EM Structure of a Functional Monomeric Photosystem
I from Thermosynechococcus Elongatus Reveals Red Chlorophyll Cluster.” Communications
Biology, vol. 4, no. 1, 304, Springer , 2021, doi:10.1038/s42003-021-01808-9.
short: M.O. Çoruh, A. Frank, H. Tanaka, A. Kawamoto, E. El-Mohsnawy, T. Kato, K.
Namba, C. Gerle, M.M. Nowaczyk, G. Kurisu, Communications Biology 4 (2021).
date_created: 2021-11-19T11:37:29Z
date_published: 2021-03-08T00:00:00Z
date_updated: 2023-08-14T11:51:19Z
day: '08'
ddc:
- '570'
department:
- _id: LeSa
doi: 10.1038/s42003-021-01808-9
external_id:
isi:
- '000627440700001'
pmid:
- '33686186'
file:
- access_level: open_access
checksum: 8ffd39f2bba7152a2441802ff313bf0b
content_type: application/pdf
creator: cchlebak
date_created: 2021-11-19T15:09:18Z
date_updated: 2021-11-19T15:09:18Z
file_id: '10318'
file_name: 2021_CommBio_Çoruh.pdf
file_size: 6030261
relation: main_file
success: 1
file_date_updated: 2021-11-19T15:09:18Z
has_accepted_license: '1'
intvolume: ' 4'
isi: 1
issue: '1'
keyword:
- general agricultural and biological Sciences
- general biochemistry
- genetics and molecular biology
- medicine (miscellaneous)
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: Communications Biology
publication_identifier:
issn:
- 2399-3642
publication_status: published
publisher: 'Springer '
quality_controlled: '1'
scopus_import: '1'
status: public
title: Cryo-EM structure of a functional monomeric Photosystem I from Thermosynechococcus
elongatus reveals red chlorophyll cluster
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: 4
year: '2021'
...
---
_id: '10406'
abstract:
- lang: eng
text: Multicellular organisms develop complex shapes from much simpler, single-celled
zygotes through a process commonly called morphogenesis. Morphogenesis involves
an interplay between several factors, ranging from the gene regulatory networks
determining cell fate and differentiation to the mechanical processes underlying
cell and tissue shape changes. Thus, the study of morphogenesis has historically
been based on multidisciplinary approaches at the interface of biology with physics
and mathematics. Recent technological advances have further improved our ability
to study morphogenesis by bridging the gap between the genetic and biophysical
factors through the development of new tools for visualizing, analyzing, and perturbing
these factors and their biochemical intermediaries. Here, we review how a combination
of genetic, microscopic, biophysical, and biochemical approaches has aided our
attempts to understand morphogenesis and discuss potential approaches that may
be beneficial to such an inquiry in the future.
acknowledgement: The authors would like to thank Feyza Nur Arslan, Suyash Naik, Diana
Pinheiro, Alexandra Schauer, and Shayan Shamipour for their comments on the draft.
N.M. is supported by an ISTplus postdoctoral fellowship (H2020 Marie-Sklodowska-Curie
COFUND Action).
article_processing_charge: No
article_type: original
author:
- first_name: Nikhil
full_name: Mishra, Nikhil
id: C4D70E82-1081-11EA-B3ED-9A4C3DDC885E
last_name: Mishra
orcid: 0000-0002-6425-5788
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Mishra N, Heisenberg C-PJ. Dissecting organismal morphogenesis by bridging
genetics and biophysics. Annual Review of Genetics. 2021;55:209-233. doi:10.1146/annurev-genet-071819-103748
apa: Mishra, N., & Heisenberg, C.-P. J. (2021). Dissecting organismal morphogenesis
by bridging genetics and biophysics. Annual Review of Genetics. Annual
Reviews. https://doi.org/10.1146/annurev-genet-071819-103748
chicago: Mishra, Nikhil, and Carl-Philipp J Heisenberg. “Dissecting Organismal Morphogenesis
by Bridging Genetics and Biophysics.” Annual Review of Genetics. Annual
Reviews, 2021. https://doi.org/10.1146/annurev-genet-071819-103748.
ieee: N. Mishra and C.-P. J. Heisenberg, “Dissecting organismal morphogenesis by
bridging genetics and biophysics,” Annual Review of Genetics, vol. 55.
Annual Reviews, pp. 209–233, 2021.
ista: Mishra N, Heisenberg C-PJ. 2021. Dissecting organismal morphogenesis by bridging
genetics and biophysics. Annual Review of Genetics. 55, 209–233.
mla: Mishra, Nikhil, and Carl-Philipp J. Heisenberg. “Dissecting Organismal Morphogenesis
by Bridging Genetics and Biophysics.” Annual Review of Genetics, vol. 55,
Annual Reviews, 2021, pp. 209–33, doi:10.1146/annurev-genet-071819-103748.
short: N. Mishra, C.-P.J. Heisenberg, Annual Review of Genetics 55 (2021) 209–233.
date_created: 2021-12-05T23:01:41Z
date_published: 2021-08-30T00:00:00Z
date_updated: 2023-08-14T13:05:13Z
day: '30'
department:
- _id: CaHe
doi: 10.1146/annurev-genet-071819-103748
ec_funded: 1
external_id:
isi:
- '000747220900010'
pmid:
- '34460295'
intvolume: ' 55'
isi: 1
keyword:
- morphogenesis
- forward genetics
- high-resolution microscopy
- biophysics
- biochemistry
- patterning
language:
- iso: eng
month: '08'
oa_version: None
page: 209-233
pmid: 1
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
publication: Annual Review of Genetics
publication_identifier:
eissn:
- 1545-2948
issn:
- 0066-4197
publication_status: published
publisher: Annual Reviews
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dissecting organismal morphogenesis by bridging genetics and biophysics
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 55
year: '2021'
...
---
_id: '12585'
abstract:
- lang: eng
text: Glaciers in High Mountain Asia generate meltwater that supports the water
needs of 250 million people, but current knowledge of annual accumulation and
ablation is limited to sparse field measurements biased in location and glacier
size. Here, we present altitudinally-resolved specific mass balances (surface,
internal, and basal combined) for 5527 glaciers in High Mountain Asia for 2000–2016,
derived by correcting observed glacier thinning patterns for mass redistribution
due to ice flow. We find that 41% of glaciers accumulated mass over less than
20% of their area, and only 60% ± 10% of regional annual ablation was compensated
by accumulation. Even without 21st century warming, 21% ± 1% of ice volume will
be lost by 2100 due to current climatic-geometric imbalance, representing a reduction
in glacier ablation into rivers of 28% ± 1%. The ablation of glaciers in the Himalayas
and Tien Shan was mostly unsustainable and ice volume in these regions will reduce
by at least 30% by 2100. The most important and vulnerable glacier-fed river basins
(Amu Darya, Indus, Syr Darya, Tarim Interior) were supplied with >50% sustainable
glacier ablation but will see long-term reductions in ice mass and glacier meltwater
supply regardless of the Karakoram Anomaly.
article_number: '2868'
article_processing_charge: No
article_type: original
author:
- first_name: Evan
full_name: Miles, Evan
last_name: Miles
- first_name: Michael
full_name: McCarthy, Michael
last_name: McCarthy
- first_name: Amaury
full_name: Dehecq, Amaury
last_name: Dehecq
- first_name: Marin
full_name: Kneib, Marin
last_name: Kneib
- first_name: Stefan
full_name: Fugger, Stefan
last_name: Fugger
- first_name: Francesca
full_name: Pellicciotti, Francesca
id: b28f055a-81ea-11ed-b70c-a9fe7f7b0e70
last_name: Pellicciotti
citation:
ama: Miles E, McCarthy M, Dehecq A, Kneib M, Fugger S, Pellicciotti F. Health and
sustainability of glaciers in High Mountain Asia. Nature Communications.
2021;12. doi:10.1038/s41467-021-23073-4
apa: Miles, E., McCarthy, M., Dehecq, A., Kneib, M., Fugger, S., & Pellicciotti,
F. (2021). Health and sustainability of glaciers in High Mountain Asia. Nature
Communications. Springer Nature. https://doi.org/10.1038/s41467-021-23073-4
chicago: Miles, Evan, Michael McCarthy, Amaury Dehecq, Marin Kneib, Stefan Fugger,
and Francesca Pellicciotti. “Health and Sustainability of Glaciers in High Mountain
Asia.” Nature Communications. Springer Nature, 2021. https://doi.org/10.1038/s41467-021-23073-4.
ieee: E. Miles, M. McCarthy, A. Dehecq, M. Kneib, S. Fugger, and F. Pellicciotti,
“Health and sustainability of glaciers in High Mountain Asia,” Nature Communications,
vol. 12. Springer Nature, 2021.
ista: Miles E, McCarthy M, Dehecq A, Kneib M, Fugger S, Pellicciotti F. 2021. Health
and sustainability of glaciers in High Mountain Asia. Nature Communications. 12,
2868.
mla: Miles, Evan, et al. “Health and Sustainability of Glaciers in High Mountain
Asia.” Nature Communications, vol. 12, 2868, Springer Nature, 2021, doi:10.1038/s41467-021-23073-4.
short: E. Miles, M. McCarthy, A. Dehecq, M. Kneib, S. Fugger, F. Pellicciotti, Nature
Communications 12 (2021).
date_created: 2023-02-20T08:11:29Z
date_published: 2021-05-17T00:00:00Z
date_updated: 2023-02-28T13:21:51Z
day: '17'
doi: 10.1038/s41467-021-23073-4
extern: '1'
intvolume: ' 12'
keyword:
- General Physics and Astronomy
- General Biochemistry
- Genetics and Molecular Biology
- General Chemistry
- Multidisciplinary
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1038/s41467-021-23073-4
month: '05'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Health and sustainability of glaciers in High Mountain Asia
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 12
year: '2021'
...
---
_id: '9778'
abstract:
- lang: eng
text: The hippocampal mossy fiber synapse is a key synapse of the trisynaptic circuit.
Post-tetanic potentiation (PTP) is the most powerful form of plasticity at this
synaptic connection. It is widely believed that mossy fiber PTP is an entirely
presynaptic phenomenon, implying that PTP induction is input-specific, and requires
neither activity of multiple inputs nor stimulation of postsynaptic neurons. To
directly test cooperativity and associativity, we made paired recordings between
single mossy fiber terminals and postsynaptic CA3 pyramidal neurons in rat brain
slices. By stimulating non-overlapping mossy fiber inputs converging onto single
CA3 neurons, we confirm that PTP is input-specific and non-cooperative. Unexpectedly,
mossy fiber PTP exhibits anti-associative induction properties. EPSCs show only
minimal PTP after combined pre- and postsynaptic high-frequency stimulation with
intact postsynaptic Ca2+ signaling, but marked PTP in the absence of postsynaptic
spiking and after suppression of postsynaptic Ca2+ signaling (10 mM EGTA). PTP
is largely recovered by inhibitors of voltage-gated R- and L-type Ca2+ channels,
group II mGluRs, and vacuolar-type H+-ATPase, suggesting the involvement of retrograde
vesicular glutamate signaling. Transsynaptic regulation of PTP extends the repertoire
of synaptic computations, implementing a brake on mossy fiber detonation and a
“smart teacher” function of hippocampal mossy fiber synapses.
acknowledged_ssus:
- _id: SSU
acknowledgement: We thank Drs. Carolina Borges-Merjane and Jose Guzman for critically
reading the manuscript, and Pablo Castillo for discussions. We are grateful to Alois
Schlögl for help with analysis, Florian Marr for excellent technical assistance
and cell reconstruction, Christina Altmutter for technical help, Eleftheria Kralli-Beller
for manuscript editing, and the Scientific Service Units of IST Austria for support.
This project received funding from the European Research Council (ERC) under the
European Union’s Horizon 2020 research and innovation program (grant agreement No
692692) and the Fond zur Förderung der Wissenschaftlichen Forschung (Z 312-B27,
Wittgenstein award), both to P.J.
article_number: '2912'
article_processing_charge: No
article_type: original
author:
- first_name: David H
full_name: Vandael, David H
id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87
last_name: Vandael
orcid: 0000-0001-7577-1676
- first_name: Yuji
full_name: Okamoto, Yuji
id: 3337E116-F248-11E8-B48F-1D18A9856A87
last_name: Okamoto
orcid: 0000-0003-0408-6094
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
citation:
ama: Vandael DH, Okamoto Y, Jonas PM. Transsynaptic modulation of presynaptic short-term
plasticity in hippocampal mossy fiber synapses. Nature Communications.
2021;12(1). doi:10.1038/s41467-021-23153-5
apa: Vandael, D. H., Okamoto, Y., & Jonas, P. M. (2021). Transsynaptic modulation
of presynaptic short-term plasticity in hippocampal mossy fiber synapses. Nature
Communications. Springer. https://doi.org/10.1038/s41467-021-23153-5
chicago: Vandael, David H, Yuji Okamoto, and Peter M Jonas. “Transsynaptic Modulation
of Presynaptic Short-Term Plasticity in Hippocampal Mossy Fiber Synapses.” Nature
Communications. Springer, 2021. https://doi.org/10.1038/s41467-021-23153-5.
ieee: D. H. Vandael, Y. Okamoto, and P. M. Jonas, “Transsynaptic modulation of presynaptic
short-term plasticity in hippocampal mossy fiber synapses,” Nature Communications,
vol. 12, no. 1. Springer, 2021.
ista: Vandael DH, Okamoto Y, Jonas PM. 2021. Transsynaptic modulation of presynaptic
short-term plasticity in hippocampal mossy fiber synapses. Nature Communications.
12(1), 2912.
mla: Vandael, David H., et al. “Transsynaptic Modulation of Presynaptic Short-Term
Plasticity in Hippocampal Mossy Fiber Synapses.” Nature Communications,
vol. 12, no. 1, 2912, Springer, 2021, doi:10.1038/s41467-021-23153-5.
short: D.H. Vandael, Y. Okamoto, P.M. Jonas, Nature Communications 12 (2021).
date_created: 2021-08-06T07:22:55Z
date_published: 2021-05-18T00:00:00Z
date_updated: 2023-08-10T14:16:16Z
day: '18'
ddc:
- '570'
department:
- _id: PeJo
doi: 10.1038/s41467-021-23153-5
ec_funded: 1
external_id:
isi:
- '000655481800014'
file:
- access_level: open_access
checksum: 6036a8cdae95e1707c2a04d54e325ff4
content_type: application/pdf
creator: kschuh
date_created: 2021-12-17T11:34:50Z
date_updated: 2021-12-17T11:34:50Z
file_id: '10563'
file_name: 2021_NatureCommunications_Vandael.pdf
file_size: 3108845
relation: main_file
success: 1
file_date_updated: 2021-12-17T11:34:50Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
issue: '1'
keyword:
- general physics and astronomy
- general biochemistry
- genetics and molecular biology
- general chemistry
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
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: 25C5A090-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z00312
name: The Wittgenstein Prize
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/synaptic-transmission-not-a-one-way-street/
scopus_import: '1'
status: public
title: Transsynaptic modulation of presynaptic short-term plasticity in hippocampal
mossy fiber synapses
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: 12
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: '11056'
abstract:
- lang: eng
text: Aging of the circulatory system correlates with the pathogenesis of a large
spectrum of diseases. However, it is largely unknown which factors drive the age-dependent
or pathological decline of the vasculature and how vascular defects relate to
tissue aging. The goal of the study is to design a multianalytical approach to
identify how the cellular microenvironment (i.e., fibroblasts) and serum from
healthy donors of different ages or Alzheimer disease (AD) patients can modulate
the functionality of organ-specific vascular endothelial cells (VECs). Long-living
human microvascular networks embedding VECs and fibroblasts from skin biopsies
are generated. RNA-seq, secretome analyses, and microfluidic assays demonstrate
that fibroblasts from young donors restore the functionality of aged endothelial
cells, an effect also achieved by serum from young donors. New biomarkers of vascular
aging are validated in human biopsies and it is shown that young serum induces
angiopoietin-like-4, which can restore compromised vascular barriers. This strategy
is then employed to characterize transcriptional/functional changes induced on
the blood–brain barrier by AD serum, demonstrating the importance of PTP4A3 in
the regulation of permeability. Features of vascular degeneration during aging
and AD are recapitulated, and a tool to identify novel biomarkers that can be
exploited to develop future therapeutics modulating vascular function is established.
article_number: '2000044'
article_processing_charge: No
article_type: original
author:
- first_name: Simone
full_name: Bersini, Simone
last_name: Bersini
- first_name: Rafael
full_name: Arrojo e Drigo, Rafael
last_name: Arrojo e Drigo
- first_name: Ling
full_name: Huang, Ling
last_name: Huang
- first_name: Maxim N.
full_name: Shokhirev, Maxim N.
last_name: Shokhirev
- 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, Arrojo e Drigo R, Huang L, Shokhirev MN, Hetzer M. Transcriptional
and functional changes of the human microvasculature during physiological aging
and Alzheimer disease. Advanced Biosystems. 2020;4(5). doi:10.1002/adbi.202000044
apa: Bersini, S., Arrojo e Drigo, R., Huang, L., Shokhirev, M. N., & Hetzer,
M. (2020). Transcriptional and functional changes of the human microvasculature
during physiological aging and Alzheimer disease. Advanced Biosystems.
Wiley. https://doi.org/10.1002/adbi.202000044
chicago: Bersini, Simone, Rafael Arrojo e Drigo, Ling Huang, Maxim N. Shokhirev,
and Martin Hetzer. “Transcriptional and Functional Changes of the Human Microvasculature
during Physiological Aging and Alzheimer Disease.” Advanced Biosystems.
Wiley, 2020. https://doi.org/10.1002/adbi.202000044.
ieee: S. Bersini, R. Arrojo e Drigo, L. Huang, M. N. Shokhirev, and M. Hetzer, “Transcriptional
and functional changes of the human microvasculature during physiological aging
and Alzheimer disease,” Advanced Biosystems, vol. 4, no. 5. Wiley, 2020.
ista: Bersini S, Arrojo e Drigo R, Huang L, Shokhirev MN, Hetzer M. 2020. Transcriptional
and functional changes of the human microvasculature during physiological aging
and Alzheimer disease. Advanced Biosystems. 4(5), 2000044.
mla: Bersini, Simone, et al. “Transcriptional and Functional Changes of the Human
Microvasculature during Physiological Aging and Alzheimer Disease.” Advanced
Biosystems, vol. 4, no. 5, 2000044, Wiley, 2020, doi:10.1002/adbi.202000044.
short: S. Bersini, R. Arrojo e Drigo, L. Huang, M.N. Shokhirev, M. Hetzer, Advanced
Biosystems 4 (2020).
date_created: 2022-04-07T07:43:57Z
date_published: 2020-05-01T00:00:00Z
date_updated: 2022-07-18T08:30:48Z
day: '01'
ddc:
- '570'
doi: 10.1002/adbi.202000044
extern: '1'
external_id:
pmid:
- '32402127'
file:
- access_level: open_access
checksum: 5584d9a1609812dc75c02ce1e35d2ec0
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T07:06:05Z
date_updated: 2022-04-08T07:06:05Z
file_id: '11134'
file_name: 2020_AdvancedBiosystems_Bersini.pdf
file_size: 2490829
relation: main_file
success: 1
file_date_updated: 2022-04-08T07:06:05Z
has_accepted_license: '1'
intvolume: ' 4'
issue: '5'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- Biomedical Engineering
- Biomaterials
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
publication: Advanced Biosystems
publication_identifier:
issn:
- 2366-7478
- 2366-7478
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Transcriptional and functional changes of the human microvasculature during
physiological aging and Alzheimer 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: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 4
year: '2020'
...
---
_id: '11058'
abstract:
- lang: eng
text: Nucleoporin 93 (Nup93) expression inversely correlates with the survival of
triple-negative breast cancer patients. However, our knowledge of Nup93 function
in breast cancer besides its role as structural component of the nuclear pore
complex is not understood. Combination of functional assays and genetic analyses
suggested that chromatin interaction of Nup93 partially modulates the expression
of genes associated with actin cytoskeleton remodeling and epithelial to mesenchymal
transition, resulting in impaired invasion of triple-negative, claudin-low breast
cancer cells. Nup93 depletion induced stress fiber formation associated with reduced
cell migration/proliferation and impaired expression of mesenchymal-like genes.
Silencing LIMCH1, a gene responsible for actin cytoskeleton remodeling and up-regulated
upon Nup93 depletion, partially restored the invasive phenotype of cancer cells.
Loss of Nup93 led to significant defects in tumor establishment/propagation in
vivo, whereas patient samples revealed that high Nup93 and low LIMCH1 expression
correlate with late tumor stage. Our approach identified Nup93 as contributor
of triple-negative, claudin-low breast cancer cell invasion and paves the way
to study the role of nuclear envelope proteins during breast cancer tumorigenesis.
article_number: e201900623
article_processing_charge: No
article_type: original
author:
- first_name: Simone
full_name: Bersini, Simone
last_name: Bersini
- first_name: Nikki K
full_name: Lytle, Nikki K
last_name: Lytle
- first_name: Roberta
full_name: Schulte, Roberta
last_name: Schulte
- first_name: Ling
full_name: Huang, Ling
last_name: Huang
- first_name: Geoffrey M
full_name: Wahl, Geoffrey M
last_name: Wahl
- 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, Lytle NK, Schulte R, Huang L, Wahl GM, Hetzer M. Nup93 regulates
breast tumor growth by modulating cell proliferation and actin cytoskeleton remodeling.
Life Science Alliance. 2020;3(1). doi:10.26508/lsa.201900623
apa: Bersini, S., Lytle, N. K., Schulte, R., Huang, L., Wahl, G. M., & Hetzer,
M. (2020). Nup93 regulates breast tumor growth by modulating cell proliferation
and actin cytoskeleton remodeling. Life Science Alliance. Life Science
Alliance. https://doi.org/10.26508/lsa.201900623
chicago: Bersini, Simone, Nikki K Lytle, Roberta Schulte, Ling Huang, Geoffrey M
Wahl, and Martin Hetzer. “Nup93 Regulates Breast Tumor Growth by Modulating Cell
Proliferation and Actin Cytoskeleton Remodeling.” Life Science Alliance.
Life Science Alliance, 2020. https://doi.org/10.26508/lsa.201900623.
ieee: S. Bersini, N. K. Lytle, R. Schulte, L. Huang, G. M. Wahl, and M. Hetzer,
“Nup93 regulates breast tumor growth by modulating cell proliferation and actin
cytoskeleton remodeling,” Life Science Alliance, vol. 3, no. 1. Life Science
Alliance, 2020.
ista: Bersini S, Lytle NK, Schulte R, Huang L, Wahl GM, Hetzer M. 2020. Nup93 regulates
breast tumor growth by modulating cell proliferation and actin cytoskeleton remodeling.
Life Science Alliance. 3(1), e201900623.
mla: Bersini, Simone, et al. “Nup93 Regulates Breast Tumor Growth by Modulating
Cell Proliferation and Actin Cytoskeleton Remodeling.” Life Science Alliance,
vol. 3, no. 1, e201900623, Life Science Alliance, 2020, doi:10.26508/lsa.201900623.
short: S. Bersini, N.K. Lytle, R. Schulte, L. Huang, G.M. Wahl, M. Hetzer, Life
Science Alliance 3 (2020).
date_created: 2022-04-07T07:44:18Z
date_published: 2020-01-01T00:00:00Z
date_updated: 2022-07-18T08:31:20Z
day: '01'
ddc:
- '570'
doi: 10.26508/lsa.201900623
extern: '1'
external_id:
pmid:
- '31959624'
file:
- access_level: open_access
checksum: 3bf33e7e93bef7823287807206b69b38
content_type: application/pdf
creator: dernst
date_created: 2022-04-08T07:33:01Z
date_updated: 2022-04-08T07:33:01Z
file_id: '11137'
file_name: 2020_LifeScienceAlliance_Bersini.pdf
file_size: 2653960
relation: main_file
success: 1
file_date_updated: 2022-04-08T07:33:01Z
has_accepted_license: '1'
intvolume: ' 3'
issue: '1'
keyword:
- Health
- Toxicology and Mutagenesis
- Plant Science
- Biochemistry
- Genetics and Molecular Biology (miscellaneous)
- Ecology
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
publication: Life Science Alliance
publication_identifier:
issn:
- 2575-1077
publication_status: published
publisher: Life Science Alliance
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nup93 regulates breast tumor growth by modulating cell proliferation and actin
cytoskeleton remodeling
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: 3
year: '2020'
...
---
_id: '8402'
abstract:
- lang: eng
text: "Background: The mitochondrial pyruvate carrier (MPC) plays a central role
in energy metabolism by transporting pyruvate across the inner mitochondrial membrane.
Its heterodimeric composition and homology to SWEET and semiSWEET transporters
set the MPC apart from the canonical mitochondrial carrier family (named MCF or
SLC25). The import of the canonical carriers is mediated by the carrier translocase
of the inner membrane (TIM22) pathway and is dependent on their structure, which
features an even number of transmembrane segments and both termini in the intermembrane
space. The import pathway of MPC proteins has not been elucidated. The odd number
of transmembrane segments and positioning of the N-terminus in the matrix argues
against an import via the TIM22 carrier pathway but favors an import via the flexible
presequence pathway.\r\nResults: Here, we systematically analyzed the import pathways
of Mpc2 and Mpc3 and report that, contrary to an expected import via the flexible
presequence pathway, yeast MPC proteins with an odd number of transmembrane segments
and matrix-exposed N-terminus are imported by the carrier pathway, using the receptor
Tom70, small TIM chaperones, and the TIM22 complex. The TIM9·10 complex chaperones
MPC proteins through the mitochondrial intermembrane space using conserved hydrophobic
motifs that are also required for the interaction with canonical carrier proteins.\r\nConclusions:
The carrier pathway can import paired and non-paired transmembrane helices and
translocate N-termini to either side of the mitochondrial inner membrane, revealing
an unexpected versatility of the mitochondrial import pathway for non-cleavable
inner membrane proteins."
article_number: '2'
article_processing_charge: No
article_type: original
author:
- first_name: Heike
full_name: Rampelt, Heike
last_name: Rampelt
- first_name: Iva
full_name: Sucec, Iva
last_name: Sucec
- first_name: Beate
full_name: Bersch, Beate
last_name: Bersch
- first_name: Patrick
full_name: Horten, Patrick
last_name: Horten
- first_name: Inge
full_name: Perschil, Inge
last_name: Perschil
- first_name: Jean-Claude
full_name: Martinou, Jean-Claude
last_name: Martinou
- first_name: Martin
full_name: van der Laan, Martin
last_name: van der Laan
- first_name: Nils
full_name: Wiedemann, Nils
last_name: Wiedemann
- first_name: Paul
full_name: Schanda, Paul
id: 7B541462-FAF6-11E9-A490-E8DFE5697425
last_name: Schanda
orcid: 0000-0002-9350-7606
- first_name: Nikolaus
full_name: Pfanner, Nikolaus
last_name: Pfanner
citation:
ama: Rampelt H, Sucec I, Bersch B, et al. The mitochondrial carrier pathway transports
non-canonical substrates with an odd number of transmembrane segments. BMC
Biology. 2020;18. doi:10.1186/s12915-019-0733-6
apa: Rampelt, H., Sucec, I., Bersch, B., Horten, P., Perschil, I., Martinou, J.-C.,
… Pfanner, N. (2020). The mitochondrial carrier pathway transports non-canonical
substrates with an odd number of transmembrane segments. BMC Biology. Springer
Nature. https://doi.org/10.1186/s12915-019-0733-6
chicago: Rampelt, Heike, Iva Sucec, Beate Bersch, Patrick Horten, Inge Perschil,
Jean-Claude Martinou, Martin van der Laan, Nils Wiedemann, Paul Schanda, and Nikolaus
Pfanner. “The Mitochondrial Carrier Pathway Transports Non-Canonical Substrates
with an Odd Number of Transmembrane Segments.” BMC Biology. Springer Nature,
2020. https://doi.org/10.1186/s12915-019-0733-6.
ieee: H. Rampelt et al., “The mitochondrial carrier pathway transports non-canonical
substrates with an odd number of transmembrane segments,” BMC Biology,
vol. 18. Springer Nature, 2020.
ista: Rampelt H, Sucec I, Bersch B, Horten P, Perschil I, Martinou J-C, van der
Laan M, Wiedemann N, Schanda P, Pfanner N. 2020. The mitochondrial carrier pathway
transports non-canonical substrates with an odd number of transmembrane segments.
BMC Biology. 18, 2.
mla: Rampelt, Heike, et al. “The Mitochondrial Carrier Pathway Transports Non-Canonical
Substrates with an Odd Number of Transmembrane Segments.” BMC Biology,
vol. 18, 2, Springer Nature, 2020, doi:10.1186/s12915-019-0733-6.
short: H. Rampelt, I. Sucec, B. Bersch, P. Horten, I. Perschil, J.-C. Martinou,
M. van der Laan, N. Wiedemann, P. Schanda, N. Pfanner, BMC Biology 18 (2020).
date_created: 2020-09-17T10:26:53Z
date_published: 2020-01-06T00:00:00Z
date_updated: 2021-01-12T08:19:02Z
day: '06'
doi: 10.1186/s12915-019-0733-6
extern: '1'
external_id:
pmid:
- '31907035'
intvolume: ' 18'
keyword:
- Biotechnology
- Plant Science
- General Biochemistry
- Genetics and Molecular Biology
- Developmental Biology
- Cell Biology
- Physiology
- Ecology
- Evolution
- Behavior and Systematics
- Structural Biology
- General Agricultural and Biological Sciences
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1186/s12915-019-0733-6
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
publication: BMC Biology
publication_identifier:
issn:
- 1741-7007
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: The mitochondrial carrier pathway transports non-canonical substrates with
an odd number of transmembrane segments
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 18
year: '2020'
...
---
_id: '8529'
abstract:
- lang: eng
text: Practical quantum networks require low-loss and noise-resilient optical interconnects
as well as non-Gaussian resources for entanglement distillation and distributed
quantum computation. The latter could be provided by superconducting circuits
but existing solutions to interface the microwave and optical domains lack either
scalability or efficiency, and in most cases the conversion noise is not known.
In this work we utilize the unique opportunities of silicon photonics, cavity
optomechanics and superconducting circuits to demonstrate a fully integrated,
coherent transducer interfacing the microwave X and the telecom S bands with a
total (internal) bidirectional transduction efficiency of 1.2% (135%) at millikelvin
temperatures. The coupling relies solely on the radiation pressure interaction
mediated by the femtometer-scale motion of two silicon nanobeams reaching a Vπ
as low as 16 μV for sub-nanowatt pump powers. Without the associated optomechanical
gain, we achieve a total (internal) pure conversion efficiency of up to 0.019%
(1.6%), relevant for future noise-free operation on this qubit-compatible platform.
acknowledged_ssus:
- _id: NanoFab
acknowledgement: We thank Yuan Chen for performing supplementary FEM simulations and
Andrew Higginbotham, Ralf Riedinger, Sungkun Hong, and Lorenzo Magrini for valuable
discussions. This work was supported by IST Austria, the IST nanofabrication facility
(NFF), the European Union’s Horizon 2020 research and innovation program under grant
agreement no. 732894 (FET Proactive HOT) and the European Research Council under
grant agreement no. 758053 (ERC StG QUNNECT). G.A. is the recipient of a DOC fellowship
of the Austrian Academy of Sciences at IST Austria. W.H. is the recipient of an
ISTplus postdoctoral fellowship with funding from the European Union’s Horizon 2020
research and innovation program under the Marie Sklodowska-Curie grant agreement
no. 754411. J.M.F. acknowledges support from the Austrian Science Fund (FWF) through
BeyondC (F71), a NOMIS foundation research grant, and the EU’s Horizon 2020 research
and innovation program under grant agreement no. 862644 (FET Open QUARTET).
article_number: '4460'
article_processing_charge: No
article_type: original
author:
- first_name: Georg M
full_name: Arnold, Georg M
id: 3770C838-F248-11E8-B48F-1D18A9856A87
last_name: Arnold
orcid: 0000-0003-1397-7876
- first_name: Matthias
full_name: Wulf, Matthias
id: 45598606-F248-11E8-B48F-1D18A9856A87
last_name: Wulf
orcid: 0000-0001-6613-1378
- first_name: Shabir
full_name: Barzanjeh, Shabir
id: 2D25E1F6-F248-11E8-B48F-1D18A9856A87
last_name: Barzanjeh
orcid: 0000-0003-0415-1423
- first_name: Elena
full_name: Redchenko, Elena
id: 2C21D6E8-F248-11E8-B48F-1D18A9856A87
last_name: Redchenko
- first_name: Alfredo R
full_name: Rueda Sanchez, Alfredo R
id: 3B82B0F8-F248-11E8-B48F-1D18A9856A87
last_name: Rueda Sanchez
orcid: 0000-0001-6249-5860
- first_name: William J
full_name: Hease, William J
id: 29705398-F248-11E8-B48F-1D18A9856A87
last_name: Hease
orcid: 0000-0001-9868-2166
- first_name: Farid
full_name: Hassani, Farid
id: 2AED110C-F248-11E8-B48F-1D18A9856A87
last_name: Hassani
orcid: 0000-0001-6937-5773
- first_name: Johannes M
full_name: Fink, Johannes M
id: 4B591CBA-F248-11E8-B48F-1D18A9856A87
last_name: Fink
orcid: 0000-0001-8112-028X
citation:
ama: Arnold GM, Wulf M, Barzanjeh S, et al. Converting microwave and telecom photons
with a silicon photonic nanomechanical interface. Nature Communications.
2020;11. doi:10.1038/s41467-020-18269-z
apa: Arnold, G. M., Wulf, M., Barzanjeh, S., Redchenko, E., Rueda Sanchez, A. R.,
Hease, W. J., … Fink, J. M. (2020). Converting microwave and telecom photons with
a silicon photonic nanomechanical interface. Nature Communications. Springer
Nature. https://doi.org/10.1038/s41467-020-18269-z
chicago: Arnold, Georg M, Matthias Wulf, Shabir Barzanjeh, Elena Redchenko, Alfredo
R Rueda Sanchez, William J Hease, Farid Hassani, and Johannes M Fink. “Converting
Microwave and Telecom Photons with a Silicon Photonic Nanomechanical Interface.”
Nature Communications. Springer Nature, 2020. https://doi.org/10.1038/s41467-020-18269-z.
ieee: G. M. Arnold et al., “Converting microwave and telecom photons with
a silicon photonic nanomechanical interface,” Nature Communications, vol.
11. Springer Nature, 2020.
ista: Arnold GM, Wulf M, Barzanjeh S, Redchenko E, Rueda Sanchez AR, Hease WJ, Hassani
F, Fink JM. 2020. Converting microwave and telecom photons with a silicon photonic
nanomechanical interface. Nature Communications. 11, 4460.
mla: Arnold, Georg M., et al. “Converting Microwave and Telecom Photons with a Silicon
Photonic Nanomechanical Interface.” Nature Communications, vol. 11, 4460,
Springer Nature, 2020, doi:10.1038/s41467-020-18269-z.
short: G.M. Arnold, M. Wulf, S. Barzanjeh, E. Redchenko, A.R. Rueda Sanchez, W.J.
Hease, F. Hassani, J.M. Fink, Nature Communications 11 (2020).
date_created: 2020-09-18T10:56:20Z
date_published: 2020-09-08T00:00:00Z
date_updated: 2024-08-07T07:11:51Z
day: '08'
ddc:
- '530'
department:
- _id: JoFi
doi: 10.1038/s41467-020-18269-z
ec_funded: 1
external_id:
isi:
- '000577280200001'
file:
- access_level: open_access
checksum: 88f92544889eb18bb38e25629a422a86
content_type: application/pdf
creator: dernst
date_created: 2020-09-18T13:02:37Z
date_updated: 2020-09-18T13:02:37Z
file_id: '8530'
file_name: 2020_NatureComm_Arnold.pdf
file_size: 1002818
relation: main_file
success: 1
file_date_updated: 2020-09-18T13:02:37Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- General Physics and Astronomy
- General Chemistry
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
project:
- _id: 257EB838-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '732894'
name: Hybrid Optomechanical Technologies
- _id: 26336814-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '758053'
name: A Fiber Optic Transceiver for Superconducting Qubits
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 237CBA6C-32DE-11EA-91FC-C7463DDC885E
call_identifier: H2020
grant_number: '862644'
name: Quantum readout techniques and technologies
- _id: 2671EB66-B435-11E9-9278-68D0E5697425
name: Coherent on-chip conversion of superconducting qubit signals from microwaves
to optical frequencies
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1038/s41467-020-18912-9
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/how-to-transport-microwave-quantum-information-via-optical-fiber/
record:
- id: '13056'
relation: research_data
status: public
status: public
title: Converting microwave and telecom photons with a silicon photonic nanomechanical
interface
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: '2020'
...
---
_id: '8568'
abstract:
- lang: eng
text: Aqueous iodine based electrochemical energy storage is considered a potential
candidate to improve sustainability and performance of current battery and supercapacitor
technology. It harnesses the redox activity of iodide, iodine, and polyiodide
species in the confined geometry of nanoporous carbon electrodes. However, current
descriptions of the electrochemical reaction mechanism to interconvert these species
are elusive. Here we show that electrochemical oxidation of iodide in nanoporous
carbons forms persistent solid iodine deposits. Confinement slows down dissolution
into triiodide and pentaiodide, responsible for otherwise significant self-discharge
via shuttling. The main tools for these insights are in situ Raman spectroscopy
and in situ small and wide-angle X-ray scattering (in situ SAXS/WAXS). In situ
Raman confirms the reversible formation of triiodide and pentaiodide. In situ
SAXS/WAXS indicates remarkable amounts of solid iodine deposited in the carbon
nanopores. Combined with stochastic modeling, in situ SAXS allows quantifying
the solid iodine volume fraction and visualizing the iodine structure on 3D lattice
models at the sub-nanometer scale. Based on the derived mechanism, we demonstrate
strategies for improved iodine pore filling capacity and prevention of self-discharge,
applicable to hybrid supercapacitors and batteries.
article_number: '4838'
article_processing_charge: No
article_type: original
author:
- first_name: Christian
full_name: Prehal, Christian
last_name: Prehal
- first_name: Harald
full_name: Fitzek, Harald
last_name: Fitzek
- first_name: Gerald
full_name: Kothleitner, Gerald
last_name: Kothleitner
- first_name: Volker
full_name: Presser, Volker
last_name: Presser
- first_name: Bernhard
full_name: Gollas, Bernhard
last_name: Gollas
- first_name: Stefan Alexander
full_name: Freunberger, Stefan Alexander
id: A8CA28E6-CE23-11E9-AD2D-EC27E6697425
last_name: Freunberger
orcid: 0000-0003-2902-5319
- first_name: Qamar
full_name: Abbas, Qamar
last_name: Abbas
citation:
ama: Prehal C, Fitzek H, Kothleitner G, et al. Persistent and reversible solid iodine
electrodeposition in nanoporous carbons. Nature Communications. 2020;11.
doi:10.1038/s41467-020-18610-6
apa: Prehal, C., Fitzek, H., Kothleitner, G., Presser, V., Gollas, B., Freunberger,
S. A., & Abbas, Q. (2020). Persistent and reversible solid iodine electrodeposition
in nanoporous carbons. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-020-18610-6
chicago: Prehal, Christian, Harald Fitzek, Gerald Kothleitner, Volker Presser, Bernhard
Gollas, Stefan Alexander Freunberger, and Qamar Abbas. “Persistent and Reversible
Solid Iodine Electrodeposition in Nanoporous Carbons.” Nature Communications.
Springer Nature, 2020. https://doi.org/10.1038/s41467-020-18610-6.
ieee: C. Prehal et al., “Persistent and reversible solid iodine electrodeposition
in nanoporous carbons,” Nature Communications, vol. 11. Springer Nature,
2020.
ista: Prehal C, Fitzek H, Kothleitner G, Presser V, Gollas B, Freunberger SA, Abbas
Q. 2020. Persistent and reversible solid iodine electrodeposition in nanoporous
carbons. Nature Communications. 11, 4838.
mla: Prehal, Christian, et al. “Persistent and Reversible Solid Iodine Electrodeposition
in Nanoporous Carbons.” Nature Communications, vol. 11, 4838, Springer
Nature, 2020, doi:10.1038/s41467-020-18610-6.
short: C. Prehal, H. Fitzek, G. Kothleitner, V. Presser, B. Gollas, S.A. Freunberger,
Q. Abbas, Nature Communications 11 (2020).
date_created: 2020-09-25T07:23:13Z
date_published: 2020-09-24T00:00:00Z
date_updated: 2023-08-22T09:37:24Z
day: '24'
ddc:
- '530'
department:
- _id: StFr
doi: 10.1038/s41467-020-18610-6
external_id:
isi:
- '000573756600004'
file:
- access_level: open_access
checksum: eada7bc8dd16a49390137cff882ef328
content_type: application/pdf
creator: dernst
date_created: 2020-09-28T13:16:15Z
date_updated: 2020-09-28T13:16:15Z
file_id: '8585'
file_name: 2020_NatureComm_Prehal.pdf
file_size: 1822469
relation: main_file
success: 1
file_date_updated: 2020-09-28T13:16:15Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
keyword:
- General Biochemistry
- Genetics and Molecular Biology
- General Physics and Astronomy
- General Chemistry
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1038/s41467-020-19720-x
status: public
title: Persistent and reversible solid iodine electrodeposition in nanoporous carbons
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: '2020'
...