---
_id: '308'
abstract:
- lang: eng
text: Migrating cells penetrate tissue barriers during development, inflammatory
responses, and tumor metastasis. We study if migration in vivo in such three-dimensionally
confined environments requires changes in the mechanical properties of the surrounding
cells using embryonic Drosophila melanogaster hemocytes, also called macrophages,
as a model. We find that macrophage invasion into the germband through transient
separation of the apposing ectoderm and mesoderm requires cell deformations and
reductions in apical tension in the ectoderm. Interestingly, the genetic pathway
governing these mechanical shifts acts downstream of the only known tumor necrosis
factor superfamily member in Drosophila, Eiger, and its receptor, Grindelwald.
Eiger-Grindelwald signaling reduces levels of active Myosin in the germband ectodermal
cortex through the localization of a Crumbs complex component, Patj (Pals-1-associated
tight junction protein). We therefore elucidate a distinct molecular pathway that
controls tissue tension and demonstrate the importance of such regulation for
invasive migration in vivo.
acknowledged_ssus:
- _id: SSU
article_processing_charge: No
article_type: original
author:
- first_name: Aparna
full_name: Ratheesh, Aparna
id: 2F064CFE-F248-11E8-B48F-1D18A9856A87
last_name: Ratheesh
orcid: 0000-0001-7190-0776
- first_name: Julia
full_name: Biebl, Julia
id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87
last_name: Biebl
- first_name: Michael
full_name: Smutny, Michael
last_name: Smutny
- first_name: Jana
full_name: Veselá, Jana
id: 433253EE-F248-11E8-B48F-1D18A9856A87
last_name: Veselá
- first_name: Ekaterina
full_name: Papusheva, Ekaterina
id: 41DB591E-F248-11E8-B48F-1D18A9856A87
last_name: Papusheva
- first_name: Gabriel
full_name: Krens, Gabriel
id: 2B819732-F248-11E8-B48F-1D18A9856A87
last_name: Krens
orcid: 0000-0003-4761-5996
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Alessandra M
full_name: Casano, Alessandra M
id: 3DBA3F4E-F248-11E8-B48F-1D18A9856A87
last_name: Casano
orcid: 0000-0002-6009-6804
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
citation:
ama: Ratheesh A, Bicher J, Smutny M, et al. Drosophila TNF modulates tissue tension
in the embryo to facilitate macrophage invasive migration. Developmental Cell.
2018;45(3):331-346. doi:10.1016/j.devcel.2018.04.002
apa: Ratheesh, A., Bicher, J., Smutny, M., Veselá, J., Papusheva, E., Krens, G.,
… Siekhaus, D. E. (2018). Drosophila TNF modulates tissue tension in the embryo
to facilitate macrophage invasive migration. Developmental Cell. Elsevier.
https://doi.org/10.1016/j.devcel.2018.04.002
chicago: Ratheesh, Aparna, Julia Bicher, Michael Smutny, Jana Veselá, Ekaterina
Papusheva, Gabriel Krens, Walter Kaufmann, Attila György, Alessandra M Casano,
and Daria E Siekhaus. “Drosophila TNF Modulates Tissue Tension in the Embryo to
Facilitate Macrophage Invasive Migration.” Developmental Cell. Elsevier,
2018. https://doi.org/10.1016/j.devcel.2018.04.002.
ieee: A. Ratheesh et al., “Drosophila TNF modulates tissue tension in the
embryo to facilitate macrophage invasive migration,” Developmental Cell,
vol. 45, no. 3. Elsevier, pp. 331–346, 2018.
ista: Ratheesh A, Bicher J, Smutny M, Veselá J, Papusheva E, Krens G, Kaufmann W,
György A, Casano AM, Siekhaus DE. 2018. Drosophila TNF modulates tissue tension
in the embryo to facilitate macrophage invasive migration. Developmental Cell.
45(3), 331–346.
mla: Ratheesh, Aparna, et al. “Drosophila TNF Modulates Tissue Tension in the Embryo
to Facilitate Macrophage Invasive Migration.” Developmental Cell, vol.
45, no. 3, Elsevier, 2018, pp. 331–46, doi:10.1016/j.devcel.2018.04.002.
short: A. Ratheesh, J. Bicher, M. Smutny, J. Veselá, E. Papusheva, G. Krens, W.
Kaufmann, A. György, A.M. Casano, D.E. Siekhaus, Developmental Cell 45 (2018)
331–346.
date_created: 2018-12-11T11:45:44Z
date_published: 2018-05-07T00:00:00Z
date_updated: 2023-09-11T13:22:13Z
day: '07'
department:
- _id: DaSi
- _id: CaHe
- _id: Bio
- _id: EM-Fac
- _id: MiSi
doi: 10.1016/j.devcel.2018.04.002
ec_funded: 1
external_id:
isi:
- '000432461400009'
pmid:
- '29738712'
intvolume: ' 45'
isi: 1
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.devcel.2018.04.002
month: '05'
oa: 1
oa_version: Published Version
page: 331 - 346
pmid: 1
project:
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: Drosophila TNFa´s Funktion in Immunzellen
- _id: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
publication: Developmental Cell
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/cells-change-tension-to-make-tissue-barriers-easier-to-get-through/
scopus_import: '1'
status: public
title: Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage
invasive migration
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 45
year: '2018'
...
---
_id: '318'
abstract:
- lang: eng
text: The insect’s fat body combines metabolic and immunological functions. In this
issue of Developmental Cell, Franz et al. (2018) show that in Drosophila, cells
of the fat body are not static, but can actively “swim” toward sites of epithelial
injury, where they physically clog the wound and locally secrete antimicrobial
peptides.
acknowledgement: Short Survey
article_processing_charge: No
author:
- first_name: Alessandra M
full_name: Casano, Alessandra M
id: 3DBA3F4E-F248-11E8-B48F-1D18A9856A87
last_name: Casano
orcid: 0000-0002-6009-6804
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Casano AM, Sixt MK. A fat lot of good for wound healing. Developmental Cell.
2018;44(4):405-406. doi:10.1016/j.devcel.2018.02.009
apa: Casano, A. M., & Sixt, M. K. (2018). A fat lot of good for wound healing.
Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2018.02.009
chicago: Casano, Alessandra M, and Michael K Sixt. “A Fat Lot of Good for Wound
Healing.” Developmental Cell. Cell Press, 2018. https://doi.org/10.1016/j.devcel.2018.02.009.
ieee: A. M. Casano and M. K. Sixt, “A fat lot of good for wound healing,” Developmental
Cell, vol. 44, no. 4. Cell Press, pp. 405–406, 2018.
ista: Casano AM, Sixt MK. 2018. A fat lot of good for wound healing. Developmental
Cell. 44(4), 405–406.
mla: Casano, Alessandra M., and Michael K. Sixt. “A Fat Lot of Good for Wound Healing.”
Developmental Cell, vol. 44, no. 4, Cell Press, 2018, pp. 405–06, doi:10.1016/j.devcel.2018.02.009.
short: A.M. Casano, M.K. Sixt, Developmental Cell 44 (2018) 405–406.
date_created: 2018-12-11T11:45:47Z
date_published: 2018-02-26T00:00:00Z
date_updated: 2023-09-08T11:42:28Z
day: '26'
department:
- _id: MiSi
doi: 10.1016/j.devcel.2018.02.009
external_id:
isi:
- '000426150700002'
pmid:
- '29486189'
intvolume: ' 44'
isi: 1
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/29486189
month: '02'
oa: 1
oa_version: Published Version
page: 405 - 406
pmid: 1
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '7547'
quality_controlled: '1'
scopus_import: '1'
status: public
title: A fat lot of good for wound healing
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 44
year: '2018'
...
---
_id: '323'
abstract:
- lang: eng
text: 'In the here presented thesis, we explore the role of branched actin networks
in cell migration and antigen presentation, the two most relevant processes in
dendritic cell biology. Branched actin networks construct lamellipodial protrusions
at the leading edge of migrating cells. These are typically seen as adhesive structures,
which mediate force transduction to the extracellular matrix that leads to forward
locomotion. We ablated Arp2/3 nucleation promoting factor WAVE in DCs and found
that the resulting cells lack lamellipodial protrusions. Instead, depending on
the maturation state, one or multiple filopodia were formed. By challenging these
cells in a variety of migration assays we found that lamellipodial protrusions
are dispensable for the locomotion of leukocytes and actually dampen the speed
of migration. However, lamellipodia are critically required to negotiate complex
environments that DCs experience while they travel to the next draining lymph
node. Taken together our results suggest that leukocyte lamellipodia have rather
a sensory- than a force transducing function. Furthermore, we show for the first
time structure and dynamics of dendritic cell F-actin at the immunological synapse
with naïve T cells. Dendritic cell F-actin appears as dynamic foci that are nucleated
by the Arp2/3 complex. WAVE ablated dendritic cells show increased membrane tension,
leading to an altered ultrastructure of the immunological synapse and severe T
cell priming defects. These results point towards a previously unappreciated role
of the cellular mechanics of dendritic cells in T cell activation. Additionally,
we present a novel cell culture based system for the differentiation of dendritic
cells from conditionally immortalized hematopoietic precursors. These precursor
cells are genetically tractable via the CRISPR/Cas9 system while they retain their
ability to differentiate into highly migratory dendritic cells and other immune
cells. This will foster the study of all aspects of dendritic cell biology and
beyond. '
acknowledged_ssus:
- _id: NanoFab
- _id: Bio
- _id: PreCl
- _id: EM-Fac
acknowledgement: "First of all I would like to thank Michael Sixt for giving me the
opportunity to work in \r\nhis group and for his support throughout the years. He
is a truly inspiring person and \r\nthe best boss one can imagine. I would
\ also like to thank all current and past \r\nmembers of the Sixt group for
their help and the great working atmosphere in the lab. \r\nIt is a true privilege
to work with such a bright, funny and friendly group of people and \r\nI’m proud
\ that I could be part of it. Furthermore, I would like to say ‘thank
\ you’ to Daria Siekhaus for all the meetings and discussion we had throughout
the years \r\nand to Federica Benvenuti for being part of my committee.
\ I am also grateful to Jack \r\nMerrin in the nanofabrication facility
\ and all the people working in the bioimaging-\r\n, the electron microscopy-
and the preclinical facilities."
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
citation:
ama: Leithner AF. Branched actin networks in dendritic cell biology. 2018. doi:10.15479/AT:ISTA:th_998
apa: Leithner, A. F. (2018). Branched actin networks in dendritic cell biology.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_998
chicago: Leithner, Alexander F. “Branched Actin Networks in Dendritic Cell Biology.”
Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_998.
ieee: A. F. Leithner, “Branched actin networks in dendritic cell biology,” Institute
of Science and Technology Austria, 2018.
ista: Leithner AF. 2018. Branched actin networks in dendritic cell biology. Institute
of Science and Technology Austria.
mla: Leithner, Alexander F. Branched Actin Networks in Dendritic Cell Biology.
Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_998.
short: A.F. Leithner, Branched Actin Networks in Dendritic Cell Biology, Institute
of Science and Technology Austria, 2018.
date_created: 2018-12-11T11:45:49Z
date_published: 2018-04-12T00:00:00Z
date_updated: 2023-09-07T12:39:44Z
day: '12'
ddc:
- '571'
- '599'
- '610'
degree_awarded: PhD
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:th_998
file:
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checksum: d5e3edbac548c26c1fa43a4b37a54a4c
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: dernst
date_created: 2019-04-05T09:23:11Z
date_updated: 2021-02-11T23:30:17Z
embargo_to: open_access
file_id: '6219'
file_name: PhD_thesis_AlexLeithner_final_version.docx
file_size: 29027671
relation: source_file
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date_created: 2019-04-05T09:23:11Z
date_updated: 2021-02-11T11:17:16Z
embargo: 2019-04-15
file_id: '6220'
file_name: PhD_thesis_AlexLeithner.pdf
file_size: 66045341
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file_date_updated: 2021-02-11T23:30:17Z
has_accepted_license: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: '99'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '7542'
pubrep_id: '998'
related_material:
record:
- id: '1321'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: Branched actin networks in dendritic cell biology
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: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2018'
...
---
_id: '402'
abstract:
- lang: eng
text: During metastasis, malignant cells escape the primary tumor, intravasate lymphatic
vessels, and reach draining sentinel lymph nodes before they colonize distant
organs via the blood circulation. Although lymph node metastasis in cancer patients
correlates with poor prognosis, evidence is lacking as to whether and how tumor
cells enter the bloodstream via lymph nodes. To investigate this question, we
delivered carcinoma cells into the lymph nodes of mice by microinfusing the cells
into afferent lymphatic vessels. We found that tumor cells rapidly infiltrated
the lymph node parenchyma, invaded blood vessels, and seeded lung metastases without
involvement of the thoracic duct. These results suggest that the lymph node blood
vessels can serve as an exit route for systemic dissemination of cancer cells
in experimental mouse models. Whether this form of tumor cell spreading occurs
in cancer patients remains to be determined.
acknowledged_ssus:
- _id: Bio
acknowledgement: "M.B. was supported by the Cell Communication in Health and Disease
graduate study program of the Austrian Science Fund (FWF) and the Medical University
of Vienna. M.S. was supported by the European Research Council (grant ERC GA 281556)
and an FWF START award.\r\nWe thank C. Moussion for establishing the intralymphatic
injection at IST Austria and for providing anti-PNAd hybridoma supernatant, R. Förster
and A. Braun for sharing the intralymphatic injection technology, K. Vaahtomeri
for the lentiviral constructs, M. Hons for establishing in vivo multiphoton imaging,
the Sixt lab for intellectual input, M. Schunn for help with the design of the in
vivo experiments, F. Langer for technical assistance with the in vivo experiments,
the bioimaging facility of IST Austria for support, and R. Efferl for providing
the CT26 cell line."
article_processing_charge: No
article_type: original
author:
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Helga
full_name: Schachner, Helga
last_name: Schachner
- first_name: Gabriele
full_name: Asfour, Gabriele
last_name: Asfour
- first_name: Zsuzsanna
full_name: Bagó Horváth, Zsuzsanna
last_name: Bagó Horváth
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- first_name: Pavel
full_name: Uhrin, Pavel
last_name: Uhrin
- 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: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
citation:
ama: Brown M, Assen FP, Leithner AF, et al. Lymph node blood vessels provide exit
routes for metastatic tumor cell dissemination in mice. Science. 2018;359(6382):1408-1411.
doi:10.1126/science.aal3662
apa: Brown, M., Assen, F. P., Leithner, A. F., Abe, J., Schachner, H., Asfour, G.,
… Kerjaschki, D. (2018). Lymph node blood vessels provide exit routes for metastatic
tumor cell dissemination in mice. Science. American Association for the
Advancement of Science. https://doi.org/10.1126/science.aal3662
chicago: Brown, Markus, Frank P Assen, Alexander F Leithner, Jun Abe, Helga Schachner,
Gabriele Asfour, Zsuzsanna Bagó Horváth, et al. “Lymph Node Blood Vessels Provide
Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” Science.
American Association for the Advancement of Science, 2018. https://doi.org/10.1126/science.aal3662.
ieee: M. Brown et al., “Lymph node blood vessels provide exit routes for
metastatic tumor cell dissemination in mice,” Science, vol. 359, no. 6382.
American Association for the Advancement of Science, pp. 1408–1411, 2018.
ista: Brown M, Assen FP, Leithner AF, Abe J, Schachner H, Asfour G, Bagó Horváth
Z, Stein J, Uhrin P, Sixt MK, Kerjaschki D. 2018. Lymph node blood vessels provide
exit routes for metastatic tumor cell dissemination in mice. Science. 359(6382),
1408–1411.
mla: Brown, Markus, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic
Tumor Cell Dissemination in Mice.” Science, vol. 359, no. 6382, American
Association for the Advancement of Science, 2018, pp. 1408–11, doi:10.1126/science.aal3662.
short: M. Brown, F.P. Assen, A.F. Leithner, J. Abe, H. Schachner, G. Asfour, Z.
Bagó Horváth, J. Stein, P. Uhrin, M.K. Sixt, D. Kerjaschki, Science 359 (2018)
1408–1411.
date_created: 2018-12-11T11:46:16Z
date_published: 2018-03-23T00:00:00Z
date_updated: 2024-03-25T23:30:05Z
day: '23'
department:
- _id: MiSi
doi: 10.1126/science.aal3662
ec_funded: 1
external_id:
isi:
- '000428043600047'
pmid:
- '29567714'
intvolume: ' 359'
isi: 1
issue: '6382'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1126/science.aal3662
month: '03'
oa: 1
oa_version: Published Version
page: 1408 - 1411
pmid: 1
project:
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7428'
quality_controlled: '1'
related_material:
record:
- id: '6947'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination
in mice
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 359
year: '2018'
...
---
_id: '437'
abstract:
- lang: eng
text: Dendritic cells (DCs) are sentinels of the adaptive immune system that reside
in peripheral organs of mammals. Upon pathogen encounter, they undergo maturation
and up-regulate the chemokine receptor CCR7 that guides them along gradients of
its chemokine ligands CCL19 and 21 to the next draining lymph node. There, DCs
present peripherally acquired antigen to naïve T cells, thereby triggering adaptive
immunity.
acknowledged_ssus:
- _id: SSU
acknowledgement: "This work was supported by grants of the European Research Council
(ERC CoG 724373) and the Austrian Science Fund (FWF) to M.S. We thank the scientific
support units at IST Austria for excellent technical support.\r\nWe thank the scientific
\ support units at IST Austria for excellent technical support. "
article_processing_charge: Yes (via OA deal)
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Hans
full_name: Haecker, Hans
last_name: Haecker
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Leithner AF, Renkawitz J, de Vries I, Hauschild R, Haecker H, Sixt MK. Fast
and efficient genetic engineering of hematopoietic precursor cells for the study
of dendritic cell migration. European Journal of Immunology. 2018;48(6):1074-1077.
doi:10.1002/eji.201747358
apa: Leithner, A. F., Renkawitz, J., de Vries, I., Hauschild, R., Haecker, H., &
Sixt, M. K. (2018). Fast and efficient genetic engineering of hematopoietic precursor
cells for the study of dendritic cell migration. European Journal of Immunology.
Wiley-Blackwell. https://doi.org/10.1002/eji.201747358
chicago: Leithner, Alexander F, Jörg Renkawitz, Ingrid de Vries, Robert Hauschild,
Hans Haecker, and Michael K Sixt. “Fast and Efficient Genetic Engineering of Hematopoietic
Precursor Cells for the Study of Dendritic Cell Migration.” European Journal
of Immunology. Wiley-Blackwell, 2018. https://doi.org/10.1002/eji.201747358.
ieee: A. F. Leithner, J. Renkawitz, I. de Vries, R. Hauschild, H. Haecker, and M.
K. Sixt, “Fast and efficient genetic engineering of hematopoietic precursor cells
for the study of dendritic cell migration,” European Journal of Immunology,
vol. 48, no. 6. Wiley-Blackwell, pp. 1074–1077, 2018.
ista: Leithner AF, Renkawitz J, de Vries I, Hauschild R, Haecker H, Sixt MK. 2018.
Fast and efficient genetic engineering of hematopoietic precursor cells for the
study of dendritic cell migration. European Journal of Immunology. 48(6), 1074–1077.
mla: Leithner, Alexander F., et al. “Fast and Efficient Genetic Engineering of Hematopoietic
Precursor Cells for the Study of Dendritic Cell Migration.” European Journal
of Immunology, vol. 48, no. 6, Wiley-Blackwell, 2018, pp. 1074–77, doi:10.1002/eji.201747358.
short: A.F. Leithner, J. Renkawitz, I. de Vries, R. Hauschild, H. Haecker, M.K.
Sixt, European Journal of Immunology 48 (2018) 1074–1077.
date_created: 2018-12-11T11:46:28Z
date_published: 2018-02-13T00:00:00Z
date_updated: 2023-09-11T14:01:18Z
day: '13'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
doi: 10.1002/eji.201747358
ec_funded: 1
external_id:
isi:
- '000434963700016'
file:
- access_level: open_access
checksum: 9d5b74cd016505aeb9a4c2d33bbedaeb
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:56Z
date_updated: 2020-07-14T12:46:27Z
file_id: '5044'
file_name: IST-2018-1067-v1+2_Leithner_et_al-2018-European_Journal_of_Immunology.pdf
file_size: 590106
relation: main_file
file_date_updated: 2020-07-14T12:46:27Z
has_accepted_license: '1'
intvolume: ' 48'
isi: 1
issue: '6'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 1074 - 1077
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
publication: European Journal of Immunology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '7386'
pubrep_id: '1067'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Fast and efficient genetic engineering of hematopoietic precursor cells for
the study of dendritic cell migration
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 48
year: '2018'
...
---
_id: '694'
abstract:
- lang: eng
text: A change regarding the extent of adhesion - hereafter referred to as adhesion
plasticity - between adhesive and less-adhesive states of mammalian cells is important
for their behavior. To investigate adhesion plasticity, we have selected a stable
isogenic subpopulation of human MDA-MB-468 breast carcinoma cells growing in suspension.
These suspension cells are unable to re-adhere to various matrices or to contract
three-dimensional collagen lattices. By using transcriptome analysis, we identified
the focal adhesion protein tensin3 (Tns3) as a determinant of adhesion plasticity.
Tns3 is strongly reduced at mRNA and protein levels in suspension cells. Furthermore,
by transiently challenging breast cancer cells to grow under non-adherent conditions
markedly reduces Tns3 protein expression, which is regained upon re-adhesion.
Stable knockdown of Tns3 in parental MDA-MB-468 cells results in defective adhesion,
spreading and migration. Tns3-knockdown cells display impaired structure and dynamics
of focal adhesion complexes as determined by immunostaining. Restoration of Tns3
protein expression in suspension cells partially rescues adhesion and focal contact
composition. Our work identifies Tns3 as a crucial focal adhesion component regulated
by, and functionally contributing to, the switch between adhesive and non-adhesive
states in MDA-MB-468 cancer cells.
article_type: original
author:
- first_name: Astrid
full_name: Veß, Astrid
last_name: Veß
- first_name: Ulrich
full_name: Blache, Ulrich
last_name: Blache
- first_name: Laura
full_name: Leitner, Laura
last_name: Leitner
- first_name: Angela
full_name: Kurz, Angela
last_name: Kurz
- first_name: Anja
full_name: Ehrenpfordt, Anja
last_name: Ehrenpfordt
- 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: Guido
full_name: Posern, Guido
last_name: Posern
citation:
ama: Veß A, Blache U, Leitner L, et al. A dual phenotype of MDA MB 468 cancer cells
reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell
Science. 2017;130(13):2172-2184. doi:10.1242/jcs.200899
apa: Veß, A., Blache, U., Leitner, L., Kurz, A., Ehrenpfordt, A., Sixt, M. K., &
Posern, G. (2017). A dual phenotype of MDA MB 468 cancer cells reveals mutual
regulation of tensin3 and adhesion plasticity. Journal of Cell Science.
Company of Biologists. https://doi.org/10.1242/jcs.200899
chicago: Veß, Astrid, Ulrich Blache, Laura Leitner, Angela Kurz, Anja Ehrenpfordt,
Michael K Sixt, and Guido Posern. “A Dual Phenotype of MDA MB 468 Cancer Cells
Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell
Science. Company of Biologists, 2017. https://doi.org/10.1242/jcs.200899.
ieee: A. Veß et al., “A dual phenotype of MDA MB 468 cancer cells reveals
mutual regulation of tensin3 and adhesion plasticity,” Journal of Cell Science,
vol. 130, no. 13. Company of Biologists, pp. 2172–2184, 2017.
ista: Veß A, Blache U, Leitner L, Kurz A, Ehrenpfordt A, Sixt MK, Posern G. 2017.
A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3
and adhesion plasticity. Journal of Cell Science. 130(13), 2172–2184.
mla: Veß, Astrid, et al. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual
Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science,
vol. 130, no. 13, Company of Biologists, 2017, pp. 2172–84, doi:10.1242/jcs.200899.
short: A. Veß, U. Blache, L. Leitner, A. Kurz, A. Ehrenpfordt, M.K. Sixt, G. Posern,
Journal of Cell Science 130 (2017) 2172–2184.
date_created: 2018-12-11T11:47:58Z
date_published: 2017-07-01T00:00:00Z
date_updated: 2021-01-12T08:09:41Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1242/jcs.200899
external_id:
pmid:
- '28515231'
file:
- access_level: open_access
checksum: 42c81a0a4fc3128883b391c3af3f74bc
content_type: application/pdf
creator: dernst
date_created: 2019-10-24T09:43:56Z
date_updated: 2020-07-14T12:47:45Z
file_id: '6966'
file_name: 2017_CellScience_Vess.pdf
file_size: 10847596
relation: main_file
file_date_updated: 2020-07-14T12:47:45Z
has_accepted_license: '1'
intvolume: ' 130'
issue: '13'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: 2172 - 2184
pmid: 1
publication: Journal of Cell Science
publication_identifier:
issn:
- '00219533'
publication_status: published
publisher: Company of Biologists
publist_id: '7008'
quality_controlled: '1'
scopus_import: 1
status: public
title: A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3
and adhesion plasticity
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 130
year: '2017'
...
---
_id: '727'
abstract:
- lang: eng
text: 'Actin filaments polymerizing against membranes power endocytosis, vesicular
traffic, and cell motility. In vitro reconstitution studies suggest that the structure
and the dynamics of actin networks respond to mechanical forces. We demonstrate
that lamellipodial actin of migrating cells responds to mechanical load when membrane
tension is modulated. In a steady state, migrating cell filaments assume the canonical
dendritic geometry, defined by Arp2/3-generated 70° branch points. Increased tension
triggers a dense network with a broadened range of angles, whereas decreased tension
causes a shift to a sparse configuration dominated by filaments growing perpendicularly
to the plasma membrane. We show that these responses emerge from the geometry
of branched actin: when load per filament decreases, elongation speed increases
and perpendicular filaments gradually outcompete others because they polymerize
the shortest distance to the membrane, where they are protected from capping.
This network-intrinsic geometrical adaptation mechanism tunes protrusive force
in response to mechanical load.'
acknowledged_ssus:
- _id: ScienComp
article_processing_charge: No
author:
- first_name: Jan
full_name: Mueller, Jan
last_name: Mueller
- first_name: Gregory
full_name: Szep, Gregory
id: 4BFB7762-F248-11E8-B48F-1D18A9856A87
last_name: Szep
- first_name: Maria
full_name: Nemethova, Maria
id: 34E27F1C-F248-11E8-B48F-1D18A9856A87
last_name: Nemethova
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Arnon
full_name: Lieber, Arnon
last_name: Lieber
- first_name: Christoph
full_name: Winkler, Christoph
last_name: Winkler
- first_name: Karsten
full_name: Kruse, Karsten
last_name: Kruse
- first_name: John
full_name: Small, John
last_name: Small
- first_name: Christian
full_name: Schmeiser, Christian
last_name: Schmeiser
- first_name: Kinneret
full_name: Keren, Kinneret
last_name: Keren
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Mueller J, Szep G, Nemethova M, et al. Load adaptation of lamellipodial actin
networks. Cell. 2017;171(1):188-200. doi:10.1016/j.cell.2017.07.051
apa: Mueller, J., Szep, G., Nemethova, M., de Vries, I., Lieber, A., Winkler, C.,
… Sixt, M. K. (2017). Load adaptation of lamellipodial actin networks. Cell.
Cell Press. https://doi.org/10.1016/j.cell.2017.07.051
chicago: Mueller, Jan, Gregory Szep, Maria Nemethova, Ingrid de Vries, Arnon Lieber,
Christoph Winkler, Karsten Kruse, et al. “Load Adaptation of Lamellipodial Actin
Networks.” Cell. Cell Press, 2017. https://doi.org/10.1016/j.cell.2017.07.051.
ieee: J. Mueller et al., “Load adaptation of lamellipodial actin networks,”
Cell, vol. 171, no. 1. Cell Press, pp. 188–200, 2017.
ista: Mueller J, Szep G, Nemethova M, de Vries I, Lieber A, Winkler C, Kruse K,
Small J, Schmeiser C, Keren K, Hauschild R, Sixt MK. 2017. Load adaptation of
lamellipodial actin networks. Cell. 171(1), 188–200.
mla: Mueller, Jan, et al. “Load Adaptation of Lamellipodial Actin Networks.” Cell,
vol. 171, no. 1, Cell Press, 2017, pp. 188–200, doi:10.1016/j.cell.2017.07.051.
short: J. Mueller, G. Szep, M. Nemethova, I. de Vries, A. Lieber, C. Winkler, K.
Kruse, J. Small, C. Schmeiser, K. Keren, R. Hauschild, M.K. Sixt, Cell 171 (2017)
188–200.
date_created: 2018-12-11T11:48:10Z
date_published: 2017-09-21T00:00:00Z
date_updated: 2023-09-28T11:33:49Z
day: '21'
department:
- _id: MiSi
- _id: Bio
doi: 10.1016/j.cell.2017.07.051
ec_funded: 1
external_id:
isi:
- '000411331800020'
intvolume: ' 171'
isi: 1
issue: '1'
language:
- iso: eng
month: '09'
oa_version: None
page: 188 - 200
project:
- _id: 25AD6156-B435-11E9-9278-68D0E5697425
grant_number: LS13-029
name: Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Cell
publication_identifier:
issn:
- '00928674'
publication_status: published
publisher: Cell Press
publist_id: '6951'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Load adaptation of lamellipodial actin networks
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 171
year: '2017'
...
---
_id: '5567'
abstract:
- lang: eng
text: Immunological synapse DC-Tcells
article_processing_charge: No
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
citation:
ama: Leithner AF. Immunological synapse DC-Tcells. 2017. doi:10.15479/AT:ISTA:71
apa: Leithner, A. F. (2017). Immunological synapse DC-Tcells. Institute of Science
and Technology Austria. https://doi.org/10.15479/AT:ISTA:71
chicago: Leithner, Alexander F. “Immunological Synapse DC-Tcells.” Institute of
Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:71.
ieee: A. F. Leithner, “Immunological synapse DC-Tcells.” Institute of Science and
Technology Austria, 2017.
ista: Leithner AF. 2017. Immunological synapse DC-Tcells, Institute of Science and
Technology Austria, 10.15479/AT:ISTA:71.
mla: Leithner, Alexander F. Immunological Synapse DC-Tcells. Institute of
Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:71.
short: A.F. Leithner, (2017).
datarep_id: '71'
date_created: 2018-12-12T12:31:34Z
date_published: 2017-08-09T00:00:00Z
date_updated: 2024-02-21T13:47:00Z
day: '09'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:71
file:
- access_level: open_access
checksum: 3d6942d47d0737d064706b5728c4d8c8
content_type: video/x-msvideo
creator: system
date_created: 2018-12-12T13:02:47Z
date_updated: 2020-07-14T12:47:04Z
file_id: '5612'
file_name: IST-2017-71-v1+1_Synapse_1.avi
file_size: 236204020
relation: main_file
- access_level: open_access
checksum: 4850006c047b0147a9e85b3c2f6f0af4
content_type: video/x-msvideo
creator: system
date_created: 2018-12-12T13:02:51Z
date_updated: 2020-07-14T12:47:04Z
file_id: '5613'
file_name: IST-2017-71-v1+2_Synapse_2.avi
file_size: 226232496
relation: main_file
file_date_updated: 2020-07-14T12:47:04Z
has_accepted_license: '1'
keyword:
- Immunological synapse
month: '08'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
status: public
title: Immunological synapse DC-Tcells
tmp:
image: /images/cc_0.png
legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode
name: Creative Commons Public Domain Dedication (CC0 1.0)
short: CC0 (1.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2017'
...
---
_id: '569'
abstract:
- lang: eng
text: The actomyosin ring generates force to ingress the cytokinetic cleavage furrow
in animal cells, yet its filament organization and the mechanism of contractility
is not well understood. We quantified actin filament order in human cells using
fluorescence polarization microscopy and found that cleavage furrow ingression
initiates by contraction of an equatorial actin network with randomly oriented
filaments. The network subsequently gradually reoriented actin filaments along
the cell equator. This strictly depended on myosin II activity, suggesting local
network reorganization by mechanical forces. Cortical laser microsurgery revealed
that during cytokinesis progression, mechanical tension increased substantially
along the direction of the cell equator, while the network contracted laterally
along the pole-to-pole axis without a detectable increase in tension. Our data
suggest that an asymmetric increase in cortical tension promotes filament reorientation
along the cytokinetic cleavage furrow, which might have implications for diverse
other biological processes involving actomyosin rings.
article_number: e30867
author:
- first_name: Felix
full_name: Spira, Felix
last_name: Spira
- first_name: Sara
full_name: Cuylen Haering, Sara
last_name: Cuylen Haering
- first_name: Shalin
full_name: Mehta, Shalin
last_name: Mehta
- first_name: Matthias
full_name: Samwer, Matthias
last_name: Samwer
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Amitabh
full_name: Verma, Amitabh
last_name: Verma
- first_name: Rudolf
full_name: Oldenbourg, Rudolf
last_name: Oldenbourg
- 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: Daniel
full_name: Gerlich, Daniel
last_name: Gerlich
citation:
ama: Spira F, Cuylen Haering S, Mehta S, et al. Cytokinesis in vertebrate cells
initiates by contraction of an equatorial actomyosin network composed of randomly
oriented filaments. eLife. 2017;6. doi:10.7554/eLife.30867
apa: Spira, F., Cuylen Haering, S., Mehta, S., Samwer, M., Reversat, A., Verma,
A., … Gerlich, D. (2017). Cytokinesis in vertebrate cells initiates by contraction
of an equatorial actomyosin network composed of randomly oriented filaments. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.30867
chicago: Spira, Felix, Sara Cuylen Haering, Shalin Mehta, Matthias Samwer, Anne
Reversat, Amitabh Verma, Rudolf Oldenbourg, Michael K Sixt, and Daniel Gerlich.
“Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin
Network Composed of Randomly Oriented Filaments.” ELife. eLife Sciences
Publications, 2017. https://doi.org/10.7554/eLife.30867.
ieee: F. Spira et al., “Cytokinesis in vertebrate cells initiates by contraction
of an equatorial actomyosin network composed of randomly oriented filaments,”
eLife, vol. 6. eLife Sciences Publications, 2017.
ista: Spira F, Cuylen Haering S, Mehta S, Samwer M, Reversat A, Verma A, Oldenbourg
R, Sixt MK, Gerlich D. 2017. Cytokinesis in vertebrate cells initiates by contraction
of an equatorial actomyosin network composed of randomly oriented filaments. eLife.
6, e30867.
mla: Spira, Felix, et al. “Cytokinesis in Vertebrate Cells Initiates by Contraction
of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.”
ELife, vol. 6, e30867, eLife Sciences Publications, 2017, doi:10.7554/eLife.30867.
short: F. Spira, S. Cuylen Haering, S. Mehta, M. Samwer, A. Reversat, A. Verma,
R. Oldenbourg, M.K. Sixt, D. Gerlich, ELife 6 (2017).
date_created: 2018-12-11T11:47:14Z
date_published: 2017-11-06T00:00:00Z
date_updated: 2023-02-23T12:30:29Z
day: '06'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.7554/eLife.30867
file:
- access_level: open_access
checksum: ba09c1451153d39e4f4b7cee013e314c
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:40Z
date_updated: 2020-07-14T12:47:10Z
file_id: '4829'
file_name: IST-2017-919-v1+1_elife-30867-figures-v1.pdf
file_size: 9666973
relation: main_file
- access_level: open_access
checksum: 01eb51f1d6ad679947415a51c988e137
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:41Z
date_updated: 2020-07-14T12:47:10Z
file_id: '4830'
file_name: IST-2017-919-v1+2_elife-30867-v1.pdf
file_size: 5951246
relation: main_file
file_date_updated: 2020-07-14T12:47:10Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '7245'
pubrep_id: '919'
quality_controlled: '1'
scopus_import: 1
status: public
title: Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin
network composed of randomly oriented filaments
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2017'
...
---
_id: '571'
abstract:
- lang: eng
text: Blood platelets are critical for hemostasis and thrombosis and play diverse
roles during immune responses. Despite these versatile tasks in mammalian biology,
their skills on a cellular level are deemed limited, mainly consisting in rolling,
adhesion, and aggregate formation. Here, we identify an unappreciated asset of
platelets and show that adherent platelets use adhesion receptors to mechanically
probe the adhesive substrate in their local microenvironment. When actomyosin-dependent
traction forces overcome substrate resistance, platelets migrate and pile up the
adhesive substrate together with any bound particulate material. They use this
ability to act as cellular scavengers, scanning the vascular surface for potential
invaders and collecting deposited bacteria. Microbe collection by migrating platelets
boosts the activity of professional phagocytes, exacerbating inflammatory tissue
injury in sepsis. This assigns platelets a central role in innate immune responses
and identifies them as potential targets to dampen inflammatory tissue damage
in clinical scenarios of severe systemic infection. In addition to their role
in thrombosis and hemostasis, platelets can also migrate to sites of infection
to help trap bacteria and clear the vascular surface.
author:
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Zerkah
full_name: Ahmad, Zerkah
last_name: Ahmad
- first_name: Gerhild
full_name: Rosenberger, Gerhild
last_name: Rosenberger
- first_name: Shuxia
full_name: Fan, Shuxia
last_name: Fan
- first_name: Leo
full_name: Nicolai, Leo
last_name: Nicolai
- first_name: Benjamin
full_name: Busch, Benjamin
last_name: Busch
- first_name: Gökce
full_name: Yavuz, Gökce
last_name: Yavuz
- first_name: Manja
full_name: Luckner, Manja
last_name: Luckner
- first_name: Hellen
full_name: Ishikawa Ankerhold, Hellen
last_name: Ishikawa Ankerhold
- first_name: Roman
full_name: Hennel, Roman
last_name: Hennel
- first_name: Alexandre
full_name: Benechet, Alexandre
last_name: Benechet
- first_name: Michael
full_name: Lorenz, Michael
last_name: Lorenz
- first_name: Sue
full_name: Chandraratne, Sue
last_name: Chandraratne
- first_name: Irene
full_name: Schubert, Irene
last_name: Schubert
- first_name: Sebastian
full_name: Helmer, Sebastian
last_name: Helmer
- first_name: Bianca
full_name: Striednig, Bianca
last_name: Striednig
- first_name: Konstantin
full_name: Stark, Konstantin
last_name: Stark
- first_name: Marek
full_name: Janko, Marek
last_name: Janko
- first_name: Ralph
full_name: Böttcher, Ralph
last_name: Böttcher
- first_name: Admar
full_name: Verschoor, Admar
last_name: Verschoor
- first_name: Catherine
full_name: Leon, Catherine
last_name: Leon
- first_name: Christian
full_name: Gachet, Christian
last_name: Gachet
- first_name: Thomas
full_name: Gudermann, Thomas
last_name: Gudermann
- first_name: Michael
full_name: Mederos Y Schnitzler, Michael
last_name: Mederos Y Schnitzler
- first_name: Zachary
full_name: Pincus, Zachary
last_name: Pincus
- first_name: Matteo
full_name: Iannacone, Matteo
last_name: Iannacone
- first_name: Rainer
full_name: Haas, Rainer
last_name: Haas
- first_name: Gerhard
full_name: Wanner, Gerhard
last_name: Wanner
- first_name: Kirsten
full_name: Lauber, Kirsten
last_name: Lauber
- 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: Steffen
full_name: Massberg, Steffen
last_name: Massberg
citation:
ama: Gärtner FR, Ahmad Z, Rosenberger G, et al. Migrating platelets are mechano
scavengers that collect and bundle bacteria. Cell Press. 2017;171(6):1368-1382.
doi:10.1016/j.cell.2017.11.001
apa: Gärtner, F. R., Ahmad, Z., Rosenberger, G., Fan, S., Nicolai, L., Busch, B.,
… Massberg, S. (2017). Migrating platelets are mechano scavengers that collect
and bundle bacteria. Cell Press. Cell Press. https://doi.org/10.1016/j.cell.2017.11.001
chicago: Gärtner, Florian R, Zerkah Ahmad, Gerhild Rosenberger, Shuxia Fan, Leo
Nicolai, Benjamin Busch, Gökce Yavuz, et al. “Migrating Platelets Are Mechano
Scavengers That Collect and Bundle Bacteria.” Cell Press. Cell Press, 2017.
https://doi.org/10.1016/j.cell.2017.11.001.
ieee: F. R. Gärtner et al., “Migrating platelets are mechano scavengers that
collect and bundle bacteria,” Cell Press, vol. 171, no. 6. Cell Press,
pp. 1368–1382, 2017.
ista: Gärtner FR, Ahmad Z, Rosenberger G, Fan S, Nicolai L, Busch B, Yavuz G, Luckner
M, Ishikawa Ankerhold H, Hennel R, Benechet A, Lorenz M, Chandraratne S, Schubert
I, Helmer S, Striednig B, Stark K, Janko M, Böttcher R, Verschoor A, Leon C, Gachet
C, Gudermann T, Mederos Y Schnitzler M, Pincus Z, Iannacone M, Haas R, Wanner
G, Lauber K, Sixt MK, Massberg S. 2017. Migrating platelets are mechano scavengers
that collect and bundle bacteria. Cell Press. 171(6), 1368–1382.
mla: Gärtner, Florian R., et al. “Migrating Platelets Are Mechano Scavengers That
Collect and Bundle Bacteria.” Cell Press, vol. 171, no. 6, Cell Press,
2017, pp. 1368–82, doi:10.1016/j.cell.2017.11.001.
short: F.R. Gärtner, Z. Ahmad, G. Rosenberger, S. Fan, L. Nicolai, B. Busch, G.
Yavuz, M. Luckner, H. Ishikawa Ankerhold, R. Hennel, A. Benechet, M. Lorenz, S.
Chandraratne, I. Schubert, S. Helmer, B. Striednig, K. Stark, M. Janko, R. Böttcher,
A. Verschoor, C. Leon, C. Gachet, T. Gudermann, M. Mederos Y Schnitzler, Z. Pincus,
M. Iannacone, R. Haas, G. Wanner, K. Lauber, M.K. Sixt, S. Massberg, Cell Press
171 (2017) 1368–1382.
date_created: 2018-12-11T11:47:15Z
date_published: 2017-11-30T00:00:00Z
date_updated: 2021-01-12T08:03:15Z
day: '30'
department:
- _id: MiSi
doi: 10.1016/j.cell.2017.11.001
ec_funded: 1
intvolume: ' 171'
issue: '6'
language:
- iso: eng
month: '11'
oa_version: None
page: 1368 - 1382
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Cell Press
publication_identifier:
issn:
- '00928674'
publication_status: published
publisher: Cell Press
publist_id: '7243'
quality_controlled: '1'
scopus_import: 1
status: public
title: Migrating platelets are mechano scavengers that collect and bundle bacteria
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 171
year: '2017'
...
---
_id: '659'
abstract:
- lang: eng
text: Migration frequently involves Rac-mediated protrusion of lamellipodia, formed
by Arp2/3 complex-dependent branching thought to be crucial for force generation
and stability of these networks. The formins FMNL2 and FMNL3 are Cdc42 effectors
targeting to the lamellipodium tip and shown here to nucleate and elongate actin
filaments with complementary activities in vitro. In migrating B16-F1 melanoma
cells, both formins contribute to the velocity of lamellipodium protrusion. Loss
of FMNL2/3 function in melanoma cells and fibroblasts reduces lamellipodial width,
actin filament density and -bundling, without changing patterns of Arp2/3 complex
incorporation. Strikingly, in melanoma cells, FMNL2/3 gene inactivation almost
completely abolishes protrusion forces exerted by lamellipodia and modifies their
ultrastructural organization. Consistently, CRISPR/Cas-mediated depletion of FMNL2/3
in fibroblasts reduces both migration and capability of cells to move against
viscous media. Together, we conclude that force generation in lamellipodia strongly
depends on FMNL formin activity, operating in addition to Arp2/3 complex-dependent
filament branching.
article_number: '14832'
article_processing_charge: No
author:
- first_name: Frieda
full_name: Kage, Frieda
last_name: Kage
- first_name: Moritz
full_name: Winterhoff, Moritz
last_name: Winterhoff
- first_name: Vanessa
full_name: Dimchev, Vanessa
last_name: Dimchev
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Tobias
full_name: Thalheim, Tobias
last_name: Thalheim
- first_name: Anika
full_name: Freise, Anika
last_name: Freise
- first_name: Stefan
full_name: Brühmann, Stefan
last_name: Brühmann
- first_name: Jana
full_name: Kollasser, Jana
last_name: Kollasser
- first_name: Jennifer
full_name: Block, Jennifer
last_name: Block
- first_name: Georgi A
full_name: Dimchev, Georgi A
last_name: Dimchev
- first_name: Matthias
full_name: Geyer, Matthias
last_name: Geyer
- first_name: Hams
full_name: Schnittler, Hams
last_name: Schnittler
- first_name: Cord
full_name: Brakebusch, Cord
last_name: Brakebusch
- first_name: Theresia
full_name: Stradal, Theresia
last_name: Stradal
- first_name: Marie
full_name: Carlier, Marie
last_name: Carlier
- 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: Josef
full_name: Käs, Josef
last_name: Käs
- first_name: Jan
full_name: Faix, Jan
last_name: Faix
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
citation:
ama: Kage F, Winterhoff M, Dimchev V, et al. FMNL formins boost lamellipodial force
generation. Nature Communications. 2017;8. doi:10.1038/ncomms14832
apa: Kage, F., Winterhoff, M., Dimchev, V., Müller, J., Thalheim, T., Freise, A.,
… Rottner, K. (2017). FMNL formins boost lamellipodial force generation. Nature
Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms14832
chicago: Kage, Frieda, Moritz Winterhoff, Vanessa Dimchev, Jan Müller, Tobias Thalheim,
Anika Freise, Stefan Brühmann, et al. “FMNL Formins Boost Lamellipodial Force
Generation.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/ncomms14832.
ieee: F. Kage et al., “FMNL formins boost lamellipodial force generation,”
Nature Communications, vol. 8. Nature Publishing Group, 2017.
ista: Kage F, Winterhoff M, Dimchev V, Müller J, Thalheim T, Freise A, Brühmann
S, Kollasser J, Block J, Dimchev GA, Geyer M, Schnittler H, Brakebusch C, Stradal
T, Carlier M, Sixt MK, Käs J, Faix J, Rottner K. 2017. FMNL formins boost lamellipodial
force generation. Nature Communications. 8, 14832.
mla: Kage, Frieda, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature
Communications, vol. 8, 14832, Nature Publishing Group, 2017, doi:10.1038/ncomms14832.
short: F. Kage, M. Winterhoff, V. Dimchev, J. Müller, T. Thalheim, A. Freise, S.
Brühmann, J. Kollasser, J. Block, G.A. Dimchev, M. Geyer, H. Schnittler, C. Brakebusch,
T. Stradal, M. Carlier, M.K. Sixt, J. Käs, J. Faix, K. Rottner, Nature Communications
8 (2017).
date_created: 2018-12-11T11:47:46Z
date_published: 2017-03-22T00:00:00Z
date_updated: 2021-01-12T08:08:06Z
day: '22'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1038/ncomms14832
file:
- access_level: open_access
checksum: dae30190291c3630e8102d8714a8d23e
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:21Z
date_updated: 2020-07-14T12:47:34Z
file_id: '5072'
file_name: IST-2017-902-v1+1_Kage_et_al-2017-Nature_Communications.pdf
file_size: 9523746
relation: main_file
file_date_updated: 2020-07-14T12:47:34Z
has_accepted_license: '1'
intvolume: ' 8'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
issn:
- '20411723'
publication_status: published
publisher: Nature Publishing Group
publist_id: '7075'
pubrep_id: '902'
quality_controlled: '1'
scopus_import: 1
status: public
title: FMNL formins boost lamellipodial force generation
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: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2017'
...
---
_id: '664'
abstract:
- lang: eng
text: Immune cells communicate using cytokine signals, but the quantitative rules
of this communication aren't clear. In this issue of Immunity, Oyler-Yaniv et
al. (2017) suggest that the distribution of a cytokine within a lymphatic organ
is primarily governed by the local density of cells consuming it.
author:
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Assen FP, Sixt MK. The dynamic cytokine niche. Immunity. 2017;46(4):519-520.
doi:10.1016/j.immuni.2017.04.006
apa: Assen, F. P., & Sixt, M. K. (2017). The dynamic cytokine niche. Immunity.
Cell Press. https://doi.org/10.1016/j.immuni.2017.04.006
chicago: Assen, Frank P, and Michael K Sixt. “The Dynamic Cytokine Niche.” Immunity.
Cell Press, 2017. https://doi.org/10.1016/j.immuni.2017.04.006.
ieee: F. P. Assen and M. K. Sixt, “The dynamic cytokine niche,” Immunity,
vol. 46, no. 4. Cell Press, pp. 519–520, 2017.
ista: Assen FP, Sixt MK. 2017. The dynamic cytokine niche. Immunity. 46(4), 519–520.
mla: Assen, Frank P., and Michael K. Sixt. “The Dynamic Cytokine Niche.” Immunity,
vol. 46, no. 4, Cell Press, 2017, pp. 519–20, doi:10.1016/j.immuni.2017.04.006.
short: F.P. Assen, M.K. Sixt, Immunity 46 (2017) 519–520.
date_created: 2018-12-11T11:47:47Z
date_published: 2017-04-18T00:00:00Z
date_updated: 2024-03-25T23:30:05Z
day: '18'
department:
- _id: MiSi
doi: 10.1016/j.immuni.2017.04.006
intvolume: ' 46'
issue: '4'
language:
- iso: eng
month: '04'
oa_version: None
page: 519 - 520
publication: Immunity
publication_identifier:
issn:
- '10747613'
publication_status: published
publisher: Cell Press
publist_id: '7065'
quality_controlled: '1'
related_material:
record:
- id: '6947'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: The dynamic cytokine niche
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 46
year: '2017'
...
---
_id: '668'
abstract:
- lang: eng
text: Macrophage filopodia, finger-like membrane protrusions, were first implicated
in phagocytosis more than 100 years ago, but little is still known about the involvement
of these actin-dependent structures in particle clearance. Using spinning disk
confocal microscopy to image filopodial dynamics in mouse resident Lifeact-EGFP
macrophages, we show that filopodia, or filopodia-like structures, support pathogen
clearance by multiple means. Filopodia supported the phagocytic uptake of bacterial
(Escherichia coli) particles by (i) capturing along the filopodial shaft and surfing
toward the cell body, the most common mode of capture; (ii) capturing via the
tip followed by retraction; (iii) combinations of surfing and retraction; or (iv)
sweeping actions. In addition, filopodia supported the uptake of zymosan (Saccharomyces
cerevisiae) particles by (i) providing fixation, (ii) capturing at the tip and
filopodia-guided actin anterograde flow with phagocytic cup formation, and (iii)
the rapid growth of new protrusions. To explore the role of filopodia-inducing
Cdc42, we generated myeloid-restricted Cdc42 knock-out mice. Cdc42-deficient macrophages
exhibited rapid phagocytic cup kinetics, but reduced particle clearance, which
could be explained by the marked rounded-up morphology of these cells. Macrophages
lacking Myo10, thought to act downstream of Cdc42, had normal morphology, motility,
and phagocytic cup formation, but displayed markedly reduced filopodia formation.
In conclusion, live-cell imaging revealed multiple mechanisms involving macrophage
filopodia in particle capture and engulfment. Cdc42 is not critical for filopodia
or phagocytic cup formation, but plays a key role in driving macrophage lamellipodial
spreading.
article_type: original
author:
- first_name: Markus
full_name: Horsthemke, Markus
last_name: Horsthemke
- first_name: Anne
full_name: Bachg, Anne
last_name: Bachg
- first_name: Katharina
full_name: Groll, Katharina
last_name: Groll
- first_name: Sven
full_name: Moyzio, Sven
last_name: Moyzio
- first_name: Barbara
full_name: Müther, Barbara
last_name: Müther
- first_name: Sandra
full_name: Hemkemeyer, Sandra
last_name: Hemkemeyer
- first_name: Roland
full_name: Wedlich Söldner, Roland
last_name: Wedlich Söldner
- 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: Sebastian
full_name: Tacke, Sebastian
last_name: Tacke
- first_name: Martin
full_name: Bähler, Martin
last_name: Bähler
- first_name: Peter
full_name: Hanley, Peter
last_name: Hanley
citation:
ama: Horsthemke M, Bachg A, Groll K, et al. Multiple roles of filopodial dynamics
in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion.
Journal of Biological Chemistry. 2017;292(17):7258-7273. doi:10.1074/jbc.M116.766923
apa: Horsthemke, M., Bachg, A., Groll, K., Moyzio, S., Müther, B., Hemkemeyer, S.,
… Hanley, P. (2017). Multiple roles of filopodial dynamics in particle capture
and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological
Chemistry. American Society for Biochemistry and Molecular Biology. https://doi.org/10.1074/jbc.M116.766923
chicago: Horsthemke, Markus, Anne Bachg, Katharina Groll, Sven Moyzio, Barbara Müther,
Sandra Hemkemeyer, Roland Wedlich Söldner, et al. “Multiple Roles of Filopodial
Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10
Deletion.” Journal of Biological Chemistry. American Society for Biochemistry
and Molecular Biology, 2017. https://doi.org/10.1074/jbc.M116.766923.
ieee: M. Horsthemke et al., “Multiple roles of filopodial dynamics in particle
capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion,” Journal
of Biological Chemistry, vol. 292, no. 17. American Society for Biochemistry
and Molecular Biology, pp. 7258–7273, 2017.
ista: Horsthemke M, Bachg A, Groll K, Moyzio S, Müther B, Hemkemeyer S, Wedlich
Söldner R, Sixt MK, Tacke S, Bähler M, Hanley P. 2017. Multiple roles of filopodial
dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10
deletion. Journal of Biological Chemistry. 292(17), 7258–7273.
mla: Horsthemke, Markus, et al. “Multiple Roles of Filopodial Dynamics in Particle
Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal
of Biological Chemistry, vol. 292, no. 17, American Society for Biochemistry
and Molecular Biology, 2017, pp. 7258–73, doi:10.1074/jbc.M116.766923.
short: M. Horsthemke, A. Bachg, K. Groll, S. Moyzio, B. Müther, S. Hemkemeyer, R.
Wedlich Söldner, M.K. Sixt, S. Tacke, M. Bähler, P. Hanley, Journal of Biological
Chemistry 292 (2017) 7258–7273.
date_created: 2018-12-11T11:47:49Z
date_published: 2017-04-28T00:00:00Z
date_updated: 2021-01-12T08:08:34Z
day: '28'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1074/jbc.M116.766923
file:
- access_level: open_access
checksum: d488162874326a4bb056065fa549dc4a
content_type: application/pdf
creator: dernst
date_created: 2019-10-24T15:25:42Z
date_updated: 2020-07-14T12:47:37Z
file_id: '6971'
file_name: 2017_JBC_Horsthemke.pdf
file_size: 5647880
relation: main_file
file_date_updated: 2020-07-14T12:47:37Z
has_accepted_license: '1'
intvolume: ' 292'
issue: '17'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 7258 - 7273
publication: Journal of Biological Chemistry
publication_identifier:
issn:
- '00219258'
publication_status: published
publisher: American Society for Biochemistry and Molecular Biology
publist_id: '7059'
quality_controlled: '1'
scopus_import: 1
status: public
title: Multiple roles of filopodial dynamics in particle capture and phagocytosis
and phenotypes of Cdc42 and Myo10 deletion
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 292
year: '2017'
...
---
_id: '672'
abstract:
- lang: eng
text: Trafficking cells frequently transmigrate through epithelial and endothelial
monolayers. How monolayers cooperate with the penetrating cells to support their
transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic
capillaries as a model system for transendothelial migration. We find that the
chemokine CCL21, which is the decisive guidance cue for intravasation, mainly
localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial
cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes
extracellularly enriched at the sites of endothelial cell-cell junctions. When
we reconstitute the transmigration process in vitro, we find that secretion of
CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and
selective calcium chelation in lymphatic endothelium attenuates transmigration.
Altogether, our data demonstrate a chemokine-mediated feedback between DCs and
lymphatic endothelium, which facilitates transendothelial migration.
article_processing_charge: Yes
author:
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
- first_name: Matthias
full_name: Mehling, Matthias
id: 3C23B994-F248-11E8-B48F-1D18A9856A87
last_name: Mehling
orcid: 0000-0001-8599-1226
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the
chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia.
Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027
apa: Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling,
M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes
dendritic cell transmigration across lymphatic endothelia. Cell Reports.
Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027
chicago: Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander
F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered
Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic
Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027.
ieee: K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21
promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports,
vol. 19, no. 5. Cell Press, pp. 902–909, 2017.
ista: Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann
W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic
cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909.
mla: Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21
Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports,
vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027.
short: K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling,
W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.
date_created: 2018-12-11T11:47:50Z
date_published: 2017-05-02T00:00:00Z
date_updated: 2023-02-23T12:50:09Z
day: '02'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
- _id: EM-Fac
doi: 10.1016/j.celrep.2017.04.027
ec_funded: 1
file:
- access_level: open_access
checksum: 8fdddaab1f1d76a6ec9ca94dcb6b07a2
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:54Z
date_updated: 2020-07-14T12:47:38Z
file_id: '5109'
file_name: IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf
file_size: 2248814
relation: main_file
file_date_updated: 2020-07-14T12:47:38Z
has_accepted_license: '1'
intvolume: ' 19'
issue: '5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 902 - 909
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Cell Reports
publication_identifier:
issn:
- '22111247'
publication_status: published
publisher: Cell Press
publist_id: '7052'
pubrep_id: '900'
quality_controlled: '1'
scopus_import: 1
status: public
title: Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration
across lymphatic endothelia
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: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2017'
...
---
_id: '674'
abstract:
- lang: eng
text: Navigation of cells along gradients of guidance cues is a determining step
in many developmental and immunological processes. Gradients can either be soluble
or immobilized to tissues as demonstrated for the haptotactic migration of dendritic
cells (DCs) toward higher concentrations of immobilized chemokine CCL21. To elucidate
how gradient characteristics govern cellular response patterns, we here introduce
an in vitro system allowing to track migratory responses of DCs to precisely controlled
immobilized gradients of CCL21. We find that haptotactic sensing depends on the
absolute CCL21 concentration and local steepness of the gradient, consistent with
a scenario where DC directionality is governed by the signal-to-noise ratio of
CCL21 binding to the receptor CCR7. We find that the conditions for optimal DC
guidance are perfectly provided by the CCL21 gradients we measure in vivo. Furthermore,
we find that CCR7 signal termination by the G-protein-coupled receptor kinase
6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient
sensing in vitro and confirm those observations in vivo. These findings suggest
that stable, tissue-bound CCL21 gradients as sustainable “roads” ensure optimal
guidance in vivo.
author:
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Veronika
full_name: Bierbaum, Veronika
id: 3FD04378-F248-11E8-B48F-1D18A9856A87
last_name: Bierbaum
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Teresa
full_name: Tarrant, Teresa
last_name: Tarrant
- first_name: Tobias
full_name: Bollenbach, Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic
chemokine gradients in a manner governed by signal to noise ratio and dependent
on GRK6. Current Biology. 2017;27(9):1314-1325. doi:10.1016/j.cub.2017.04.004
apa: Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries,
I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients
in a manner governed by signal to noise ratio and dependent on GRK6. Current
Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.04.004
chicago: Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus
Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret
Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio
and Dependent on GRK6.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.04.004.
ieee: J. Schwarz et al., “Dendritic cells interpret haptotactic chemokine
gradients in a manner governed by signal to noise ratio and dependent on GRK6,”
Current Biology, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017.
ista: Schwarz J, Bierbaum V, Vaahtomeri K, Hauschild R, Brown M, de Vries I, Leithner
AF, Reversat A, Merrin J, Tarrant T, Bollenbach MT, Sixt MK. 2017. Dendritic cells
interpret haptotactic chemokine gradients in a manner governed by signal to noise
ratio and dependent on GRK6. Current Biology. 27(9), 1314–1325.
mla: Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients
in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current
Biology, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:10.1016/j.cub.2017.04.004.
short: J. Schwarz, V. Bierbaum, K. Vaahtomeri, R. Hauschild, M. Brown, I. de Vries,
A.F. Leithner, A. Reversat, J. Merrin, T. Tarrant, M.T. Bollenbach, M.K. Sixt,
Current Biology 27 (2017) 1314–1325.
date_created: 2018-12-11T11:47:51Z
date_published: 2017-05-09T00:00:00Z
date_updated: 2023-02-23T12:50:44Z
day: '09'
department:
- _id: MiSi
- _id: Bio
- _id: NanoFab
doi: 10.1016/j.cub.2017.04.004
ec_funded: 1
intvolume: ' 27'
issue: '9'
language:
- iso: eng
month: '05'
oa_version: None
page: 1314 - 1325
project:
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Current Biology
publication_identifier:
issn:
- '09609822'
publication_status: published
publisher: Cell Press
publist_id: '7050'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dendritic cells interpret haptotactic chemokine gradients in a manner governed
by signal to noise ratio and dependent on GRK6
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 27
year: '2017'
...
---
_id: '677'
abstract:
- lang: eng
text: The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler
that acts in transcription, replication, and genome stability. It is required
for resistance against genotoxic agents and is involved in the repair of DNA double-strand
breaks (DSBs) by homologous recombination (HR). However, the causes of the HR
defect in INO80-C mutant cells are controversial. Here, we unite previous findings
using a system to study HR with high spatial resolution in budding yeast. We find
that INO80-C has at least two distinct functions during HR—DNA end resection and
presynaptic filament formation. Importantly, the second function is linked to
the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation
and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic
filament formation is the crucial INO80-C function during HR.
author:
- first_name: Claudio
full_name: Lademann, Claudio
last_name: Lademann
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Boris
full_name: Pfander, Boris
last_name: Pfander
- first_name: Stefan
full_name: Jentsch, Stefan
last_name: Jentsch
citation:
ama: Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z
to promote presynaptic filament formation during homologous recombination. Cell
Reports. 2017;19(7):1294-1303. doi:10.1016/j.celrep.2017.04.051
apa: Lademann, C., Renkawitz, J., Pfander, B., & Jentsch, S. (2017). The INO80
complex removes H2A.Z to promote presynaptic filament formation during homologous
recombination. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.051
chicago: Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The
INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous
Recombination.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.051.
ieee: C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex
removes H2A.Z to promote presynaptic filament formation during homologous recombination,”
Cell Reports, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017.
ista: Lademann C, Renkawitz J, Pfander B, Jentsch S. 2017. The INO80 complex removes
H2A.Z to promote presynaptic filament formation during homologous recombination.
Cell Reports. 19(7), 1294–1303.
mla: Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic
Filament Formation during Homologous Recombination.” Cell Reports, vol.
19, no. 7, Cell Press, 2017, pp. 1294–303, doi:10.1016/j.celrep.2017.04.051.
short: C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017)
1294–1303.
date_created: 2018-12-11T11:47:52Z
date_published: 2017-05-16T00:00:00Z
date_updated: 2021-01-12T08:08:57Z
day: '16'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.celrep.2017.04.051
file:
- access_level: open_access
checksum: efc7287d9c6354983cb151880e9ad72a
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:48Z
date_updated: 2020-07-14T12:47:40Z
file_id: '5171'
file_name: IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf
file_size: 3005610
relation: main_file
file_date_updated: 2020-07-14T12:47:40Z
has_accepted_license: '1'
intvolume: ' 19'
issue: '7'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 1294 - 1303
publication: Cell Reports
publication_identifier:
issn:
- '22111247'
publication_status: published
publisher: Cell Press
publist_id: '7046'
pubrep_id: '899'
quality_controlled: '1'
scopus_import: 1
status: public
title: The INO80 complex removes H2A.Z to promote presynaptic filament formation during
homologous recombination
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 19
year: '2017'
...
---
_id: '679'
abstract:
- lang: eng
text: Protective responses against pathogens require a rapid mobilization of resting
neutrophils and the timely removal of activated ones. Neutrophils are exceptionally
short-lived leukocytes, yet it remains unclear whether the lifespan of pathogen-engaged
neutrophils is regulated differently from that in the circulating steady-state
pool. Here, we have found that under homeostatic conditions, the mRNA-destabilizing
protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated
infiltrating murine neutrophils but not neutrophil cellularity. Activated TTP-deficient
neutrophils exhibited decreased apoptosis and enhanced accumulation at the infection
site. In the context of myeloid-specific deletion of Ttp, the potentiation of
neutrophil deployment protected mice against lethal soft tissue infection with
Streptococcus pyogenes and prevented bacterial dissemination. Neutrophil transcriptome
analysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically
associated with elevated expression of myeloid cell leukemia 1 (Mcl1) but not
other antiapoptotic B cell leukemia/ lymphoma 2 (Bcl2) family members. Higher
Mcl1 expression resulted from stabilization of Mcl1 mRNA in the absence of TTP.
The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable
to that of transgenic Mcl1-overexpressing neutrophils. Our study demonstrates
that posttranscriptional gene regulation by TTP schedules the termination of the
antimicrobial engagement of neutrophils. The balancing role of TTP comes at the
cost of an increased risk of bacterial infections.
acknowledgement: This work was supported by grants from the Austrian Science Fund
(FWF) (P27538-B21, I1621-B22, and SFB 43, to PK); by funding from the European Union
Seventh Framework Programme Marie Curie Initial Training Networks (FP7-PEOPLE-2012-ITN)
for the project INBIONET (INfection BIOlogy Training NETwork under grant agreement
PITN-GA-2012-316682; and by a joint research cluster initiative of the University
of Vienna and the Medical University of Vienna.
author:
- first_name: Florian
full_name: Ebner, Florian
last_name: Ebner
- first_name: Vitaly
full_name: Sedlyarov, Vitaly
last_name: Sedlyarov
- first_name: Saren
full_name: Tasciyan, Saren
id: 4323B49C-F248-11E8-B48F-1D18A9856A87
last_name: Tasciyan
orcid: 0000-0003-1671-393X
- first_name: Masa
full_name: Ivin, Masa
last_name: Ivin
- first_name: Franz
full_name: Kratochvill, Franz
last_name: Kratochvill
- first_name: Nina
full_name: Gratz, Nina
last_name: Gratz
- first_name: Lukas
full_name: Kenner, Lukas
last_name: Kenner
- first_name: Andreas
full_name: Villunger, Andreas
last_name: Villunger
- 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: Pavel
full_name: Kovarik, Pavel
last_name: Kovarik
citation:
ama: Ebner F, Sedlyarov V, Tasciyan S, et al. The RNA-binding protein tristetraprolin
schedules apoptosis of pathogen-engaged neutrophils during bacterial infection.
The Journal of Clinical Investigation. 2017;127(6):2051-2065. doi:10.1172/JCI80631
apa: Ebner, F., Sedlyarov, V., Tasciyan, S., Ivin, M., Kratochvill, F., Gratz, N.,
… Kovarik, P. (2017). The RNA-binding protein tristetraprolin schedules apoptosis
of pathogen-engaged neutrophils during bacterial infection. The Journal of
Clinical Investigation. American Society for Clinical Investigation. https://doi.org/10.1172/JCI80631
chicago: Ebner, Florian, Vitaly Sedlyarov, Saren Tasciyan, Masa Ivin, Franz Kratochvill,
Nina Gratz, Lukas Kenner, Andreas Villunger, Michael K Sixt, and Pavel Kovarik.
“The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged
Neutrophils during Bacterial Infection.” The Journal of Clinical Investigation.
American Society for Clinical Investigation, 2017. https://doi.org/10.1172/JCI80631.
ieee: F. Ebner et al., “The RNA-binding protein tristetraprolin schedules
apoptosis of pathogen-engaged neutrophils during bacterial infection,” The
Journal of Clinical Investigation, vol. 127, no. 6. American Society for Clinical
Investigation, pp. 2051–2065, 2017.
ista: Ebner F, Sedlyarov V, Tasciyan S, Ivin M, Kratochvill F, Gratz N, Kenner L,
Villunger A, Sixt MK, Kovarik P. 2017. The RNA-binding protein tristetraprolin
schedules apoptosis of pathogen-engaged neutrophils during bacterial infection.
The Journal of Clinical Investigation. 127(6), 2051–2065.
mla: Ebner, Florian, et al. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis
of Pathogen-Engaged Neutrophils during Bacterial Infection.” The Journal of
Clinical Investigation, vol. 127, no. 6, American Society for Clinical Investigation,
2017, pp. 2051–65, doi:10.1172/JCI80631.
short: F. Ebner, V. Sedlyarov, S. Tasciyan, M. Ivin, F. Kratochvill, N. Gratz, L.
Kenner, A. Villunger, M.K. Sixt, P. Kovarik, The Journal of Clinical Investigation
127 (2017) 2051–2065.
date_created: 2018-12-11T11:47:53Z
date_published: 2017-06-01T00:00:00Z
date_updated: 2024-03-25T23:30:12Z
day: '01'
department:
- _id: MiSi
doi: 10.1172/JCI80631
external_id:
pmid:
- '28504646'
intvolume: ' 127'
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451238/
month: '06'
oa: 1
oa_version: Submitted Version
page: 2051 - 2065
pmid: 1
project:
- _id: 25985A36-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T00817-B21
name: The biochemical basis of PAR polarization
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
publication: The Journal of Clinical Investigation
publication_identifier:
issn:
- '00219738'
publication_status: published
publisher: American Society for Clinical Investigation
publist_id: '7038'
quality_controlled: '1'
related_material:
record:
- id: '12401'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged
neutrophils during bacterial infection
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 127
year: '2017'
...
---
_id: '1161'
abstract:
- lang: eng
text: Coordinated changes of cell shape are often the result of the excitable, wave-like
dynamics of the actin cytoskeleton. New work shows that, in migrating cells, protrusion
waves arise from mechanochemical crosstalk between adhesion sites, membrane tension
and the actin protrusive machinery.
article_processing_charge: No
author:
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Müller J, Sixt MK. Cell migration: Making the waves. Current Biology.
2017;27(1):R24-R25. doi:10.1016/j.cub.2016.11.035'
apa: 'Müller, J., & Sixt, M. K. (2017). Cell migration: Making the waves. Current
Biology. Cell Press. https://doi.org/10.1016/j.cub.2016.11.035'
chicago: 'Müller, Jan, and Michael K Sixt. “Cell Migration: Making the Waves.” Current
Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2016.11.035.'
ieee: 'J. Müller and M. K. Sixt, “Cell migration: Making the waves,” Current
Biology, vol. 27, no. 1. Cell Press, pp. R24–R25, 2017.'
ista: 'Müller J, Sixt MK. 2017. Cell migration: Making the waves. Current Biology.
27(1), R24–R25.'
mla: 'Müller, Jan, and Michael K. Sixt. “Cell Migration: Making the Waves.” Current
Biology, vol. 27, no. 1, Cell Press, 2017, pp. R24–25, doi:10.1016/j.cub.2016.11.035.'
short: J. Müller, M.K. Sixt, Current Biology 27 (2017) R24–R25.
date_created: 2018-12-11T11:50:29Z
date_published: 2017-01-09T00:00:00Z
date_updated: 2023-09-20T11:28:19Z
day: '09'
department:
- _id: MiSi
doi: 10.1016/j.cub.2016.11.035
external_id:
isi:
- '000391902500010'
intvolume: ' 27'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: R24 - R25
publication: Current Biology
publication_identifier:
issn:
- '09609822'
publication_status: published
publisher: Cell Press
publist_id: '6197'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Cell migration: Making the waves'
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 27
year: '2017'
...
---
_id: '1217'
abstract:
- lang: eng
text: Understanding the regulation of T-cell responses during inflammation and auto-immunity
is fundamental for designing efficient therapeutic strategies against immune diseases.
In this regard, prostaglandin E 2 (PGE 2) is mostly considered a myeloid-derived
immunosuppressive molecule. We describe for the first time that T cells secrete
PGE 2 during T-cell receptor stimulation. In addition, we show that autocrine
PGE 2 signaling through EP receptors is essential for optimal CD4 + T-cell activation
in vitro and in vivo, and for T helper 1 (Th1) and regulatory T cell differentiation.
PGE 2 was found to provide additive co-stimulatory signaling through AKT activation.
Intravital multiphoton microscopy showed that triggering EP receptors in T cells
is also essential for the stability of T cell-dendritic cell (DC) interactions
and Th-cell accumulation in draining lymph nodes (LNs) during inflammation. We
further demonstrated that blocking EP receptors in T cells during the initial
phase of collagen-induced arthritis in mice resulted in a reduction of clinical
arthritis. This could be attributable to defective T-cell activation, accompanied
by a decline in activated and interferon-γ-producing CD4 + Th1 cells in draining
LNs. In conclusion, we prove that T lymphocytes secret picomolar concentrations
of PGE 2, which in turn provide additive co-stimulatory signaling, enabling T
cells to attain a favorable activation threshold. PGE 2 signaling in T cells is
also required for maintaining long and stable interactions with DCs within LNs.
Blockade of EP receptors in vivo impairs T-cell activation and development of
T cell-mediated inflammatory responses. This may have implications in various
pathophysiological settings.
acknowledgement: This manuscript has been supported by grants SAF2007-61716 and S-SAL-0159/2006
awarded by the Spanish Ministry of Science and Education and the Community of Madrid
to Dr M Fresno.
author:
- first_name: Vinatha
full_name: Sreeramkumar, Vinatha
last_name: Sreeramkumar
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Carmen
full_name: Punzón, Carmen
last_name: Punzón
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- first_name: David
full_name: Sancho, David
last_name: Sancho
- first_name: Manuel
full_name: Fresno Forcelledo, Manuel
last_name: Fresno Forcelledo
- first_name: Natalia
full_name: Cuesta, Natalia
last_name: Cuesta
citation:
ama: Sreeramkumar V, Hons M, Punzón C, et al. Efficient T-cell priming and activation
requires signaling through prostaglandin E2 (EP) receptors. Immunology and
Cell Biology. 2016;94(1):39-51. doi:10.1038/icb.2015.62
apa: Sreeramkumar, V., Hons, M., Punzón, C., Stein, J., Sancho, D., Fresno Forcelledo,
M., & Cuesta, N. (2016). Efficient T-cell priming and activation requires
signaling through prostaglandin E2 (EP) receptors. Immunology and Cell Biology.
Nature Publishing Group. https://doi.org/10.1038/icb.2015.62
chicago: Sreeramkumar, Vinatha, Miroslav Hons, Carmen Punzón, Jens Stein, David
Sancho, Manuel Fresno Forcelledo, and Natalia Cuesta. “Efficient T-Cell Priming
and Activation Requires Signaling through Prostaglandin E2 (EP) Receptors.” Immunology
and Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/icb.2015.62.
ieee: V. Sreeramkumar et al., “Efficient T-cell priming and activation requires
signaling through prostaglandin E2 (EP) receptors,” Immunology and Cell Biology,
vol. 94, no. 1. Nature Publishing Group, pp. 39–51, 2016.
ista: Sreeramkumar V, Hons M, Punzón C, Stein J, Sancho D, Fresno Forcelledo M,
Cuesta N. 2016. Efficient T-cell priming and activation requires signaling through
prostaglandin E2 (EP) receptors. Immunology and Cell Biology. 94(1), 39–51.
mla: Sreeramkumar, Vinatha, et al. “Efficient T-Cell Priming and Activation Requires
Signaling through Prostaglandin E2 (EP) Receptors.” Immunology and Cell Biology,
vol. 94, no. 1, Nature Publishing Group, 2016, pp. 39–51, doi:10.1038/icb.2015.62.
short: V. Sreeramkumar, M. Hons, C. Punzón, J. Stein, D. Sancho, M. Fresno Forcelledo,
N. Cuesta, Immunology and Cell Biology 94 (2016) 39–51.
date_created: 2018-12-11T11:50:46Z
date_published: 2016-01-01T00:00:00Z
date_updated: 2021-01-12T06:49:09Z
day: '01'
department:
- _id: MiSi
doi: 10.1038/icb.2015.62
intvolume: ' 94'
issue: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: 39 - 51
publication: Immunology and Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '6116'
quality_controlled: '1'
scopus_import: 1
status: public
title: Efficient T-cell priming and activation requires signaling through prostaglandin
E2 (EP) receptors
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 94
year: '2016'
...
---
_id: '1285'
abstract:
- lang: eng
text: Cell migration is central to a multitude of physiological processes, including
embryonic development, immune surveillance, and wound healing, and deregulated
migration is key to cancer dissemination. Decades of investigations have uncovered
many of the molecular and physical mechanisms underlying cell migration. Together
with protrusion extension and cell body retraction, adhesion to the substrate
via specific focal adhesion points has long been considered an essential step
in cell migration. Although this is true for cells moving on two-dimensional substrates,
recent studies have demonstrated that focal adhesions are not required for cells
moving in three dimensions, in which confinement is sufficient to maintain a cell
in contact with its substrate. Here, we review the investigations that have led
to challenging the requirement of specific adhesions for migration, discuss the
physical mechanisms proposed for cell body translocation during focal adhesion-independent
migration, and highlight the remaining open questions for the future.
acknowledgement: We would like to thank Dani Bodor for critical comments on the manuscript
and Guillaume Salbreux for discussions. The authors are supported by the United
Kingdom's Medical Research Council (MRC) (E.K.P. and I.M.A.; core funding to the
MRC Laboratory for Molecular Cell Biology), by the European Research Council [ERC
GA 311637 (E.K.P.) and ERC GA 281556 (M.S.)], and by a START award from the Austrian
Science Foundation (M.S.).
author:
- first_name: Ewa
full_name: Paluch, Ewa
last_name: Paluch
- first_name: Irene
full_name: Aspalter, Irene
last_name: Aspalter
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Paluch E, Aspalter I, Sixt MK. Focal adhesion-independent cell migration. Annual
Review of Cell and Developmental Biology. 2016;32:469-490. doi:10.1146/annurev-cellbio-111315-125341
apa: Paluch, E., Aspalter, I., & Sixt, M. K. (2016). Focal adhesion-independent
cell migration. Annual Review of Cell and Developmental Biology. Annual
Reviews. https://doi.org/10.1146/annurev-cellbio-111315-125341
chicago: Paluch, Ewa, Irene Aspalter, and Michael K Sixt. “Focal Adhesion-Independent
Cell Migration.” Annual Review of Cell and Developmental Biology. Annual
Reviews, 2016. https://doi.org/10.1146/annurev-cellbio-111315-125341.
ieee: E. Paluch, I. Aspalter, and M. K. Sixt, “Focal adhesion-independent cell migration,”
Annual Review of Cell and Developmental Biology, vol. 32. Annual Reviews,
pp. 469–490, 2016.
ista: Paluch E, Aspalter I, Sixt MK. 2016. Focal adhesion-independent cell migration.
Annual Review of Cell and Developmental Biology. 32, 469–490.
mla: Paluch, Ewa, et al. “Focal Adhesion-Independent Cell Migration.” Annual
Review of Cell and Developmental Biology, vol. 32, Annual Reviews, 2016, pp.
469–90, doi:10.1146/annurev-cellbio-111315-125341.
short: E. Paluch, I. Aspalter, M.K. Sixt, Annual Review of Cell and Developmental
Biology 32 (2016) 469–490.
date_created: 2018-12-11T11:51:08Z
date_published: 2016-10-06T00:00:00Z
date_updated: 2021-01-12T06:49:37Z
day: '06'
department:
- _id: MiSi
doi: 10.1146/annurev-cellbio-111315-125341
ec_funded: 1
intvolume: ' 32'
language:
- iso: eng
month: '10'
oa_version: None
page: 469 - 490
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and transduction of leukocytes (FWF)
publication: Annual Review of Cell and Developmental Biology
publication_status: published
publisher: Annual Reviews
publist_id: '6031'
quality_controlled: '1'
scopus_import: 1
status: public
title: Focal adhesion-independent cell migration
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 32
year: '2016'
...