---
_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
license: https://creativecommons.org/publicdomain/zero/1.0/
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
article_processing_charge: No
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: 2025-09-11T07:41:10Z
day: '06'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.7554/eLife.30867
external_id:
isi:
- '000414407700001'
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'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
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.
article_processing_charge: No
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: 2025-09-11T07:39:45Z
day: '30'
department:
- _id: MiSi
doi: 10.1016/j.cell.2017.11.001
ec_funded: 1
external_id:
isi:
- '000417362700018'
intvolume: ' 171'
isi: 1
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:
- 0092-8674
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
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: 2025-09-11T07:09:28Z
day: '22'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1038/ncomms14832
external_id:
isi:
- '000396993700001'
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'
isi: 1
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 8
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_processing_charge: No
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: 2025-09-11T07:03:17Z
day: '28'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1074/jbc.M116.766923
external_id:
isi:
- '000400478300035'
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'
isi: 1
issue: '17'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 7258 - 7273
publication: Journal of Biological Chemistry
publication_identifier:
issn:
- 0021-9258
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
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
orcid: 0000-0002-1073-744X
- 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.
corr_author: '1'
date_created: 2018-12-11T11:47:50Z
date_published: 2017-05-02T00:00:00Z
date_updated: 2025-09-10T14:27:34Z
day: '02'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
- _id: EM-Fac
doi: 10.1016/j.celrep.2017.04.027
ec_funded: 1
external_id:
isi:
- '000402124100002'
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'
isi: 1
issue: '5'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
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
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and force transduction of migrating leukocytes
publication: Cell Reports
publication_identifier:
issn:
- 2211-1247
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
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.
article_processing_charge: No
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
orcid: 0000-0002-1073-744X
- 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.
corr_author: '1'
date_created: 2018-12-11T11:47:51Z
date_published: 2017-05-09T00:00:00Z
date_updated: 2025-09-10T14:26:47Z
day: '09'
department:
- _id: MiSi
- _id: Bio
- _id: NanoFab
doi: 10.1016/j.cub.2017.04.004
ec_funded: 1
external_id:
isi:
- '000400741700021'
intvolume: ' 27'
isi: 1
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 force transduction of migrating leukocytes
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
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.
article_processing_charge: No
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: 2025-09-10T14:23:55Z
day: '16'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.celrep.2017.04.051
external_id:
isi:
- '000402125100002'
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'
isi: 1
issue: '7'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 1294 - 1303
publication: Cell Reports
publication_identifier:
issn:
- 2211-1247
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 19
year: '2017'
...
---
_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_processing_charge: No
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: 2025-09-10T11:13:35Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1242/jcs.200899
external_id:
isi:
- '000405612200009'
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'
isi: 1
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:
- 0021-9533
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
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.
corr_author: '1'
date_created: 2018-12-11T11:48:10Z
date_published: 2017-09-21T00:00:00Z
date_updated: 2025-07-10T11:54:27Z
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
publication: Cell
publication_identifier:
issn:
- 0092-8674
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 171
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.
article_processing_charge: No
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.
corr_author: '1'
date_created: 2018-12-11T11:47:47Z
date_published: 2017-04-18T00:00:00Z
date_updated: 2026-06-05T22:34:18Z
day: '18'
department:
- _id: MiSi
doi: 10.1016/j.immuni.2017.04.006
external_id:
isi:
- '000399451100002'
intvolume: ' 46'
isi: 1
issue: '4'
language:
- iso: eng
month: '04'
oa_version: None
page: 519 - 520
publication: Immunity
publication_identifier:
issn:
- 1074-7613
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 46
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.
article_processing_charge: No
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: 2026-06-05T22:34:43Z
day: '01'
department:
- _id: MiSi
doi: 10.1172/JCI80631
external_id:
isi:
- '000402620800008'
pmid:
- '28504646'
intvolume: ' 127'
isi: 1
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:
- 0021-9738
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 127
year: '2017'
...
---
_id: '1150'
abstract:
- lang: eng
text: When neutrophils infiltrate a site of inflammation, they have to stop at the
right place to exert their effector function. In this issue of Developmental Cell,
Wang et al. (2016) show that neutrophils sense reactive oxygen species via the
TRPM2 channel to arrest migration at their target site. © 2016 Elsevier Inc.
article_processing_charge: No
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- 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: Renkawitz J, Sixt MK. A Radical Break Restraining Neutrophil Migration. Developmental
Cell. 2016;38(5):448-450. doi:10.1016/j.devcel.2016.08.017
apa: Renkawitz, J., & Sixt, M. K. (2016). A Radical Break Restraining Neutrophil
Migration. Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2016.08.017
chicago: Renkawitz, Jörg, and Michael K Sixt. “A Radical Break Restraining Neutrophil
Migration.” Developmental Cell. Cell Press, 2016. https://doi.org/10.1016/j.devcel.2016.08.017.
ieee: J. Renkawitz and M. K. Sixt, “A Radical Break Restraining Neutrophil Migration,”
Developmental Cell, vol. 38, no. 5. Cell Press, pp. 448–450, 2016.
ista: Renkawitz J, Sixt MK. 2016. A Radical Break Restraining Neutrophil Migration.
Developmental Cell. 38(5), 448–450.
mla: Renkawitz, Jörg, and Michael K. Sixt. “A Radical Break Restraining Neutrophil
Migration.” Developmental Cell, vol. 38, no. 5, Cell Press, 2016, pp. 448–50,
doi:10.1016/j.devcel.2016.08.017.
short: J. Renkawitz, M.K. Sixt, Developmental Cell 38 (2016) 448–450.
date_created: 2018-12-11T11:50:25Z
date_published: 2016-09-12T00:00:00Z
date_updated: 2025-09-22T09:57:46Z
day: '12'
department:
- _id: MiSi
doi: 10.1016/j.devcel.2016.08.017
external_id:
isi:
- '000383413000003'
intvolume: ' 38'
isi: 1
issue: '5'
language:
- iso: eng
month: '09'
oa_version: None
page: 448 - 450
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '6208'
quality_controlled: '1'
scopus_import: '1'
status: public
title: A Radical Break Restraining Neutrophil Migration
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 38
year: '2016'
...
---
_id: '1154'
abstract:
- lang: eng
text: "Cellular locomotion is a central hallmark of eukaryotic life. It is governed
by cell-extrinsic molecular factors, which can either emerge in the soluble phase
or as immobilized, often adhesive ligands. To encode for direction, every cue
must be present as a spatial or temporal gradient. Here, we developed a microfluidic
chamber that allows measurement of cell migration in combined response to surface
immobilized and soluble molecular gradients. As a proof of principle we study
the response of dendritic cells to their major guidance cues, chemokines. The
majority of data on chemokine gradient sensing is based on in vitro studies employing
soluble gradients. Despite evidence suggesting that in vivo chemokines are often
immobilized to sugar residues, limited information is available how cells respond
to immobilized chemokines. We tracked migration of dendritic cells towards immobilized
gradients of the chemokine CCL21 and varying superimposed soluble gradients of
CCL19. Differential migratory patterns illustrate the potential of our setup to
quantitatively study the competitive response to both types of gradients. Beyond
chemokines our approach is broadly applicable to alternative systems of chemo-
and haptotaxis such as cells migrating along gradients of adhesion receptor ligands
vs. any soluble cue. \r\n"
acknowledgement: 'This work was supported by the Swiss National Science Foundation
(Ambizione fellowship; PZ00P3-154733 to M.M.), the Swiss Multiple Sclerosis Society
(research support to M.M.), a fellowship from the Boehringer Ingelheim Fonds (BIF)
to J.S., the European Research Council (grant ERC GA 281556) and a START award from
the Austrian Science Foundation (FWF) to M.S. #BioimagingFacility'
article_number: '36440'
article_processing_charge: No
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: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Tino
full_name: Frank, Tino
last_name: Frank
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Savaş
full_name: Tay, Savaş
last_name: Tay
- 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: Matthias
full_name: Mehling, Matthias
id: 3C23B994-F248-11E8-B48F-1D18A9856A87
last_name: Mehling
orcid: 0000-0001-8599-1226
citation:
ama: Schwarz J, Bierbaum V, Merrin J, et al. A microfluidic device for measuring
cell migration towards substrate bound and soluble chemokine gradients. Scientific
Reports. 2016;6. doi:10.1038/srep36440
apa: Schwarz, J., Bierbaum, V., Merrin, J., Frank, T., Hauschild, R., Bollenbach,
M. T., … Mehling, M. (2016). A microfluidic device for measuring cell migration
towards substrate bound and soluble chemokine gradients. Scientific Reports.
Nature Publishing Group. https://doi.org/10.1038/srep36440
chicago: Schwarz, Jan, Veronika Bierbaum, Jack Merrin, Tino Frank, Robert Hauschild,
Mark Tobias Bollenbach, Savaş Tay, Michael K Sixt, and Matthias Mehling. “A Microfluidic
Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine
Gradients.” Scientific Reports. Nature Publishing Group, 2016. https://doi.org/10.1038/srep36440.
ieee: J. Schwarz et al., “A microfluidic device for measuring cell migration
towards substrate bound and soluble chemokine gradients,” Scientific Reports,
vol. 6. Nature Publishing Group, 2016.
ista: Schwarz J, Bierbaum V, Merrin J, Frank T, Hauschild R, Bollenbach MT, Tay
S, Sixt MK, Mehling M. 2016. A microfluidic device for measuring cell migration
towards substrate bound and soluble chemokine gradients. Scientific Reports. 6,
36440.
mla: Schwarz, Jan, et al. “A Microfluidic Device for Measuring Cell Migration towards
Substrate Bound and Soluble Chemokine Gradients.” Scientific Reports, vol.
6, 36440, Nature Publishing Group, 2016, doi:10.1038/srep36440.
short: J. Schwarz, V. Bierbaum, J. Merrin, T. Frank, R. Hauschild, M.T. Bollenbach,
S. Tay, M.K. Sixt, M. Mehling, Scientific Reports 6 (2016).
date_created: 2018-12-11T11:50:27Z
date_published: 2016-11-07T00:00:00Z
date_updated: 2025-09-22T09:56:13Z
day: '07'
ddc:
- '579'
department:
- _id: MiSi
- _id: NanoFab
- _id: Bio
- _id: ToBo
doi: 10.1038/srep36440
ec_funded: 1
external_id:
isi:
- '000387118300001'
file:
- access_level: open_access
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:32Z
date_updated: 2018-12-12T10:09:32Z
file_id: '4756'
file_name: IST-2017-744-v1+1_srep36440.pdf
file_size: 2353456
relation: main_file
file_date_updated: 2018-12-12T10:09:32Z
has_accepted_license: '1'
intvolume: ' 6'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and force transduction of migrating leukocytes
publication: Scientific Reports
publication_status: published
publisher: Nature Publishing Group
publist_id: '6204'
pubrep_id: '744'
quality_controlled: '1'
scopus_import: '1'
status: public
title: A microfluidic device for measuring cell migration towards substrate bound
and soluble chemokine gradients
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 6
year: '2016'
...
---
_id: '1201'
abstract:
- lang: eng
text: In this issue of Cell, Skau et al. show that the formin FMN2 organizes a perinuclear
actin cytoskeleton that protects the nucleus and its genomic content of migrating
cells squeezing through small spaces.
article_processing_charge: No
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- 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: Renkawitz J, Sixt MK. Formin’ a nuclear protection. Cell. 2016;167(6):1448-1449.
doi:10.1016/j.cell.2016.11.024
apa: Renkawitz, J., & Sixt, M. K. (2016). Formin’ a nuclear protection. Cell.
Cell Press. https://doi.org/10.1016/j.cell.2016.11.024
chicago: Renkawitz, Jörg, and Michael K Sixt. “Formin’ a Nuclear Protection.” Cell.
Cell Press, 2016. https://doi.org/10.1016/j.cell.2016.11.024.
ieee: J. Renkawitz and M. K. Sixt, “Formin’ a nuclear protection,” Cell,
vol. 167, no. 6. Cell Press, pp. 1448–1449, 2016.
ista: Renkawitz J, Sixt MK. 2016. Formin’ a nuclear protection. Cell. 167(6), 1448–1449.
mla: Renkawitz, Jörg, and Michael K. Sixt. “Formin’ a Nuclear Protection.” Cell,
vol. 167, no. 6, Cell Press, 2016, pp. 1448–49, doi:10.1016/j.cell.2016.11.024.
short: J. Renkawitz, M.K. Sixt, Cell 167 (2016) 1448–1449.
date_created: 2018-12-11T11:50:41Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2025-09-22T09:41:33Z
day: '01'
department:
- _id: MiSi
doi: 10.1016/j.cell.2016.11.024
external_id:
isi:
- '000389470500007'
intvolume: ' 167'
isi: 1
issue: '6'
language:
- iso: eng
month: '12'
oa_version: None
page: 1448 - 1449
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '6149'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Formin’ a nuclear protection
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 167
year: '2016'
...
---
_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.
article_processing_charge: No
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: 2025-09-22T09:34:26Z
day: '01'
department:
- _id: MiSi
doi: 10.1038/icb.2015.62
external_id:
isi:
- '000367628600005'
intvolume: ' 94'
isi: 1
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
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.).
article_processing_charge: No
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: 2025-09-22T08:33:40Z
day: '06'
department:
- _id: MiSi
doi: 10.1146/annurev-cellbio-111315-125341
ec_funded: 1
external_id:
isi:
- '000389576900019'
intvolume: ' 32'
isi: 1
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
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and force transduction of migrating leukocytes
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 32
year: '2016'
...
---
_id: '1490'
abstract:
- lang: eng
text: To induce adaptive immunity, dendritic cells (DCs) migrate through afferent
lymphatic vessels (LVs) to draining lymph nodes (dLNs). This process occurs in
several consecutive steps. Upon entry into lymphatic capillaries, DCs first actively
crawl into downstream collecting vessels. From there, they are next passively
and rapidly transported to the dLN by lymph flow. Here, we describe a role for
the chemokine CCL21 in intralymphatic DC crawling. Performing time-lapse imaging
in murine skin, we found that blockade of CCL21-but not the absence of lymph flow-completely
abolished DC migration from capillaries toward collecting vessels and reduced
the ability of intralymphatic DCs to emigrate from skin. Moreover, we found that
in vitro low laminar flow established a CCL21 gradient along lymphatic endothelial
monolayers, thereby inducing downstream-directed DC migration. These findings
reveal a role for intralymphatic CCL21 in promoting DC trafficking to dLNs, through
the formation of a flow-induced gradient.
article_processing_charge: No
author:
- first_name: Erica
full_name: Russo, Erica
last_name: Russo
- first_name: Alvaro
full_name: Teijeira, Alvaro
last_name: Teijeira
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Ann
full_name: Willrodt, Ann
last_name: Willrodt
- first_name: Joël
full_name: Bloch, Joël
last_name: Bloch
- first_name: Maximilian
full_name: Nitschké, Maximilian
last_name: Nitschké
- first_name: Laura
full_name: Santambrogio, Laura
last_name: Santambrogio
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
- 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: Cornelia
full_name: Halin, Cornelia
last_name: Halin
citation:
ama: Russo E, Teijeira A, Vaahtomeri K, et al. Intralymphatic CCL21 promotes tissue
egress of dendritic cells through afferent lymphatic vessels. Cell Reports.
2016;14(7):1723-1734. doi:10.1016/j.celrep.2016.01.048
apa: Russo, E., Teijeira, A., Vaahtomeri, K., Willrodt, A., Bloch, J., Nitschké,
M., … Halin, C. (2016). Intralymphatic CCL21 promotes tissue egress of dendritic
cells through afferent lymphatic vessels. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2016.01.048
chicago: Russo, Erica, Alvaro Teijeira, Kari Vaahtomeri, Ann Willrodt, Joël Bloch,
Maximilian Nitschké, Laura Santambrogio, Dontscho Kerjaschki, Michael K Sixt,
and Cornelia Halin. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic
Cells through Afferent Lymphatic Vessels.” Cell Reports. Cell Press, 2016.
https://doi.org/10.1016/j.celrep.2016.01.048.
ieee: E. Russo et al., “Intralymphatic CCL21 promotes tissue egress of dendritic
cells through afferent lymphatic vessels,” Cell Reports, vol. 14, no. 7.
Cell Press, pp. 1723–1734, 2016.
ista: Russo E, Teijeira A, Vaahtomeri K, Willrodt A, Bloch J, Nitschké M, Santambrogio
L, Kerjaschki D, Sixt MK, Halin C. 2016. Intralymphatic CCL21 promotes tissue
egress of dendritic cells through afferent lymphatic vessels. Cell Reports. 14(7),
1723–1734.
mla: Russo, Erica, et al. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic
Cells through Afferent Lymphatic Vessels.” Cell Reports, vol. 14, no. 7,
Cell Press, 2016, pp. 1723–34, doi:10.1016/j.celrep.2016.01.048.
short: E. Russo, A. Teijeira, K. Vaahtomeri, A. Willrodt, J. Bloch, M. Nitschké,
L. Santambrogio, D. Kerjaschki, M.K. Sixt, C. Halin, Cell Reports 14 (2016) 1723–1734.
date_created: 2018-12-11T11:52:19Z
date_published: 2016-02-23T00:00:00Z
date_updated: 2025-09-18T11:16:44Z
day: '23'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.celrep.2016.01.048
external_id:
isi:
- '000370970200016'
file:
- access_level: open_access
checksum: c98c1151d5f1e5ce1643a83d8d7f3c29
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:12:30Z
date_updated: 2020-07-14T12:44:58Z
file_id: '4948'
file_name: IST-2016-515-v1+1_1-s2.0-S2211124716300262-main.pdf
file_size: 5489897
relation: main_file
file_date_updated: 2020-07-14T12:44:58Z
has_accepted_license: '1'
intvolume: ' 14'
isi: 1
issue: '7'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 1723 - 1734
publication: Cell Reports
publication_status: published
publisher: Cell Press
publist_id: '5697'
pubrep_id: '515'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent
lymphatic vessels
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 14
year: '2016'
...
---
_id: '1137'
abstract:
- lang: eng
text: RASGRP1 is an important guanine nucleotide exchange factor and activator of
the RAS-MAPK pathway following T cell antigen receptor (TCR) signaling. The consequences
of RASGRP1 mutations in humans are unknown. In a patient with recurrent bacterial
and viral infections, born to healthy consanguineous parents, we used homozygosity
mapping and exome sequencing to identify a biallelic stop-gain variant in RASGRP1.
This variant segregated perfectly with the disease and has not been reported in
genetic databases. RASGRP1 deficiency was associated in T cells and B cells with
decreased phosphorylation of the extracellular-signal-regulated serine kinase
ERK, which was restored following expression of wild-type RASGRP1. RASGRP1 deficiency
also resulted in defective proliferation, activation and motility of T cells and
B cells. RASGRP1-deficient natural killer (NK) cells exhibited impaired cytotoxicity
with defective granule convergence and actin accumulation. Interaction proteomics
identified the dynein light chain DYNLL1 as interacting with RASGRP1, which links
RASGRP1 to cytoskeletal dynamics. RASGRP1-deficient cells showed decreased activation
of the GTPase RhoA. Treatment with lenalidomide increased RhoA activity and reversed
the migration and activation defects of RASGRP1-deficient lymphocytes.
article_processing_charge: No
article_type: original
author:
- first_name: Elisabeth
full_name: Salzer, Elisabeth
last_name: Salzer
- first_name: Deniz
full_name: Çaǧdaş, Deniz
last_name: Çaǧdaş
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Emily
full_name: Mace, Emily
last_name: Mace
- first_name: Wojciech
full_name: Garncarz, Wojciech
last_name: Garncarz
- first_name: Oezlem
full_name: Petronczki, Oezlem
last_name: Petronczki
- first_name: René
full_name: Platzer, René
last_name: Platzer
- first_name: Laurène
full_name: Pfajfer, Laurène
last_name: Pfajfer
- first_name: Ivan
full_name: Bilic, Ivan
last_name: Bilic
- first_name: Sol
full_name: Ban, Sol
last_name: Ban
- first_name: Katharina
full_name: Willmann, Katharina
last_name: Willmann
- first_name: Malini
full_name: Mukherjee, Malini
last_name: Mukherjee
- first_name: Verena
full_name: Supper, Verena
last_name: Supper
- first_name: Hsiangting
full_name: Hsu, Hsiangting
last_name: Hsu
- first_name: Pinaki
full_name: Banerjee, Pinaki
last_name: Banerjee
- first_name: Papiya
full_name: Sinha, Papiya
last_name: Sinha
- first_name: Fabienne
full_name: Mcclanahan, Fabienne
last_name: Mcclanahan
- first_name: Gerhard
full_name: Zlabinger, Gerhard
last_name: Zlabinger
- first_name: Winfried
full_name: Pickl, Winfried
last_name: Pickl
- first_name: John
full_name: Gribben, John
last_name: Gribben
- first_name: Hannes
full_name: Stockinger, Hannes
last_name: Stockinger
- first_name: Keiryn
full_name: Bennett, Keiryn
last_name: Bennett
- first_name: Johannes
full_name: Huppa, Johannes
last_name: Huppa
- first_name: Loï̈C
full_name: Dupré, Loï̈C
last_name: Dupré
- first_name: Özden
full_name: Sanal, Özden
last_name: Sanal
- first_name: Ulrich
full_name: Jäger, Ulrich
last_name: Jäger
- 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: Ilhan
full_name: Tezcan, Ilhan
last_name: Tezcan
- first_name: Jordan
full_name: Orange, Jordan
last_name: Orange
- first_name: Kaan
full_name: Boztug, Kaan
last_name: Boztug
citation:
ama: Salzer E, Çaǧdaş D, Hons M, et al. RASGRP1 deficiency causes immunodeficiency
with impaired cytoskeletal dynamics. Nature Immunology. 2016;17(12):1352-1360.
doi:10.1038/ni.3575
apa: Salzer, E., Çaǧdaş, D., Hons, M., Mace, E., Garncarz, W., Petronczki, O., …
Boztug, K. (2016). RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal
dynamics. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3575
chicago: Salzer, Elisabeth, Deniz Çaǧdaş, Miroslav Hons, Emily Mace, Wojciech Garncarz,
Oezlem Petronczki, René Platzer, et al. “RASGRP1 Deficiency Causes Immunodeficiency
with Impaired Cytoskeletal Dynamics.” Nature Immunology. Nature Publishing
Group, 2016. https://doi.org/10.1038/ni.3575.
ieee: E. Salzer et al., “RASGRP1 deficiency causes immunodeficiency with
impaired cytoskeletal dynamics,” Nature Immunology, vol. 17, no. 12. Nature
Publishing Group, pp. 1352–1360, 2016.
ista: Salzer E, Çaǧdaş D, Hons M, Mace E, Garncarz W, Petronczki O, Platzer R, Pfajfer
L, Bilic I, Ban S, Willmann K, Mukherjee M, Supper V, Hsu H, Banerjee P, Sinha
P, Mcclanahan F, Zlabinger G, Pickl W, Gribben J, Stockinger H, Bennett K, Huppa
J, Dupré L, Sanal Ö, Jäger U, Sixt MK, Tezcan I, Orange J, Boztug K. 2016. RASGRP1
deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature
Immunology. 17(12), 1352–1360.
mla: Salzer, Elisabeth, et al. “RASGRP1 Deficiency Causes Immunodeficiency with
Impaired Cytoskeletal Dynamics.” Nature Immunology, vol. 17, no. 12, Nature
Publishing Group, 2016, pp. 1352–60, doi:10.1038/ni.3575.
short: E. Salzer, D. Çaǧdaş, M. Hons, E. Mace, W. Garncarz, O. Petronczki, R. Platzer,
L. Pfajfer, I. Bilic, S. Ban, K. Willmann, M. Mukherjee, V. Supper, H. Hsu, P.
Banerjee, P. Sinha, F. Mcclanahan, G. Zlabinger, W. Pickl, J. Gribben, H. Stockinger,
K. Bennett, J. Huppa, L. Dupré, Ö. Sanal, U. Jäger, M.K. Sixt, I. Tezcan, J. Orange,
K. Boztug, Nature Immunology 17 (2016) 1352–1360.
date_created: 2018-12-11T11:50:21Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2025-09-22T14:13:22Z
day: '01'
department:
- _id: MiSi
doi: 10.1038/ni.3575
external_id:
isi:
- '000388056400005'
pmid:
- '27776107'
intvolume: ' 17'
isi: 1
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6400263
month: '12'
oa: 1
oa_version: Submitted Version
page: 1352 - 1360
pmid: 1
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '6221'
quality_controlled: '1'
scopus_import: '1'
status: public
title: RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 17
year: '2016'
...
---
_id: '1142'
abstract:
- lang: eng
text: Hemolysis drives susceptibility to bacterial infections and predicts poor
outcome from sepsis. These detrimental effects are commonly considered to be a
consequence of heme-iron serving as a nutrient for bacteria. We employed a Gram-negative
sepsis model and found that elevated heme levels impaired the control of bacterial
proliferation independently of heme-iron acquisition by pathogens. Heme strongly
inhibited phagocytosis and the migration of human and mouse phagocytes by disrupting
actin cytoskeletal dynamics via activation of the GTP-binding Rho family protein
Cdc42 by the guanine nucleotide exchange factor DOCK8. A chemical screening approach
revealed that quinine effectively prevented heme effects on the cytoskeleton,
restored phagocytosis and improved survival in sepsis. These mechanistic insights
provide potential therapeutic targets for patients with sepsis or hemolytic disorders.
acknowledgement: 'Y. Fukui (Medical Institute of Bioregulation, Kyushu University)
and J. Stein (Theodor Kocher Institute, University of Bern) are acknowledged for
providing the DOCK8 deficient bone marrow. and H. Häcker (St. Judes Children''s
Research Hospital) for providing the ERHBD-HoxB8-encoding retroviral construct.
pSpCas9(BB)-2a-Puro (PX459) was a gift from F. Zhang (Massachusetts Institute of
Technology) (Addgene plasmid # 48139) and pGRG36 was a gift from N. Craig (Johns
Hopkins University School of Medicine) (Addgene plasmid # 16666). LifeAct-GFP-encoding
retrovirus was kindly provided by A. Leithner (Institute of Science and Technology
Austria). pSIM8 and TKC E. coli were gifts from D.L. Court (Center for Cancer Research,
National Cancer Institute). We acknowledge M. Gröger and S. Rauscher for excellent
technical support (Core imaging facility, Medical University of Vienna). We thank
D.P. Barlow and L.R. Cheever for critical reading of the manuscript. This work was
supported by the Austrian Academy of Sciences, the Science Fund of the Austrian
National Bank (14107) and the Austrian Science Fund FWF (I1620-B22) in the Infect-ERA
framework (to S.Knapp).'
article_processing_charge: No
author:
- first_name: Rui
full_name: Martins, Rui
last_name: Martins
- first_name: Julia
full_name: Maier, Julia
last_name: Maier
- first_name: Anna
full_name: Gorki, Anna
last_name: Gorki
- first_name: Kilian
full_name: Huber, Kilian
last_name: Huber
- first_name: Omar
full_name: Sharif, Omar
last_name: Sharif
- first_name: Philipp
full_name: Starkl, Philipp
last_name: Starkl
- first_name: Simona
full_name: Saluzzo, Simona
last_name: Saluzzo
- first_name: Federica
full_name: Quattrone, Federica
last_name: Quattrone
- first_name: Riem
full_name: Gawish, Riem
last_name: Gawish
- first_name: Karin
full_name: Lakovits, Karin
last_name: Lakovits
- first_name: Michael
full_name: Aichinger, Michael
last_name: Aichinger
- first_name: Branka
full_name: Radic Sarikas, Branka
last_name: Radic Sarikas
- first_name: Charles
full_name: Lardeau, Charles
last_name: Lardeau
- first_name: Anastasiya
full_name: Hladik, Anastasiya
last_name: Hladik
- first_name: Ana
full_name: Korosec, Ana
last_name: Korosec
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Michelle
full_name: Duggan, Michelle
id: 2EDEA62C-F248-11E8-B48F-1D18A9856A87
last_name: Duggan
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
- first_name: Harald
full_name: Esterbauer, Harald
last_name: Esterbauer
- first_name: Jacques
full_name: Colinge, Jacques
last_name: Colinge
- first_name: Stephanie
full_name: Eisenbarth, Stephanie
last_name: Eisenbarth
- first_name: Thomas
full_name: Decker, Thomas
last_name: Decker
- first_name: Keiryn
full_name: Bennett, Keiryn
last_name: Bennett
- first_name: Stefan
full_name: Kubicek, Stefan
last_name: Kubicek
- 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: Giulio
full_name: Superti Furga, Giulio
last_name: Superti Furga
- first_name: Sylvia
full_name: Knapp, Sylvia
last_name: Knapp
citation:
ama: Martins R, Maier J, Gorki A, et al. Heme drives hemolysis-induced susceptibility
to infection via disruption of phagocyte functions. Nature Immunology.
2016;17(12):1361-1372. doi:10.1038/ni.3590
apa: Martins, R., Maier, J., Gorki, A., Huber, K., Sharif, O., Starkl, P., … Knapp,
S. (2016). Heme drives hemolysis-induced susceptibility to infection via disruption
of phagocyte functions. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3590
chicago: Martins, Rui, Julia Maier, Anna Gorki, Kilian Huber, Omar Sharif, Philipp
Starkl, Simona Saluzzo, et al. “Heme Drives Hemolysis-Induced Susceptibility to
Infection via Disruption of Phagocyte Functions.” Nature Immunology. Nature
Publishing Group, 2016. https://doi.org/10.1038/ni.3590.
ieee: R. Martins et al., “Heme drives hemolysis-induced susceptibility to
infection via disruption of phagocyte functions,” Nature Immunology, vol.
17, no. 12. Nature Publishing Group, pp. 1361–1372, 2016.
ista: Martins R, Maier J, Gorki A, Huber K, Sharif O, Starkl P, Saluzzo S, Quattrone
F, Gawish R, Lakovits K, Aichinger M, Radic Sarikas B, Lardeau C, Hladik A, Korosec
A, Brown M, Vaahtomeri K, Duggan M, Kerjaschki D, Esterbauer H, Colinge J, Eisenbarth
S, Decker T, Bennett K, Kubicek S, Sixt MK, Superti Furga G, Knapp S. 2016. Heme
drives hemolysis-induced susceptibility to infection via disruption of phagocyte
functions. Nature Immunology. 17(12), 1361–1372.
mla: Martins, Rui, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection
via Disruption of Phagocyte Functions.” Nature Immunology, vol. 17, no.
12, Nature Publishing Group, 2016, pp. 1361–72, doi:10.1038/ni.3590.
short: R. Martins, J. Maier, A. Gorki, K. Huber, O. Sharif, P. Starkl, S. Saluzzo,
F. Quattrone, R. Gawish, K. Lakovits, M. Aichinger, B. Radic Sarikas, C. Lardeau,
A. Hladik, A. Korosec, M. Brown, K. Vaahtomeri, M. Duggan, D. Kerjaschki, H. Esterbauer,
J. Colinge, S. Eisenbarth, T. Decker, K. Bennett, S. Kubicek, M.K. Sixt, G. Superti
Furga, S. Knapp, Nature Immunology 17 (2016) 1361–1372.
date_created: 2018-12-11T11:50:22Z
date_published: 2016-12-01T00:00:00Z
date_updated: 2025-09-22T14:10:50Z
day: '01'
department:
- _id: MiSi
- _id: PeJo
doi: 10.1038/ni.3590
external_id:
isi:
- '000388056400006'
intvolume: ' 17'
isi: 1
issue: '12'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://ora.ox.ac.uk/objects/uuid:f53a464e-1e5b-4f08-a7d8-b6749b852b9d
month: '12'
oa: 1
oa_version: Submitted Version
page: 1361 - 1372
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '6216'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Heme drives hemolysis-induced susceptibility to infection via disruption of
phagocyte functions
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 17
year: '2016'
...