---
_id: '6328'
abstract:
- lang: eng
text: During metazoan development, immune surveillance and cancer dissemination,
cells migrate in complex three-dimensional microenvironments1,2,3. These spaces
are crowded by cells and extracellular matrix, generating mazes with differently
sized gaps that are typically smaller than the diameter of the migrating cell4,5.
Most mesenchymal and epithelial cells and some—but not all—cancer cells actively
generate their migratory path using pericellular tissue proteolysis6. By contrast,
amoeboid cells such as leukocytes use non-destructive strategies of locomotion7,
raising the question how these extremely fast cells navigate through dense tissues.
Here we reveal that leukocytes sample their immediate vicinity for large pore
sizes, and are thereby able to choose the path of least resistance. This allows
them to circumnavigate local obstacles while effectively following global directional
cues such as chemotactic gradients. Pore-size discrimination is facilitated by
frontward positioning of the nucleus, which enables the cells to use their bulkiest
compartment as a mechanical gauge. Once the nucleus and the closely associated
microtubule organizing centre pass the largest pore, cytoplasmic protrusions still
lingering in smaller pores are retracted. These retractions are coordinated by
dynamic microtubules; when microtubules are disrupted, migrating cells lose coherence
and frequently fragment into migratory cytoplasmic pieces. As nuclear positioning
in front of the microtubule organizing centre is a typical feature of amoeboid
migration, our findings link the fundamental organization of cellular polarity
to the strategy of locomotion.
acknowledged_ssus:
- _id: SSU
article_processing_charge: No
article_type: letter_note
author:
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- first_name: Julian A
full_name: Stopp, Julian A
id: 489E3F00-F248-11E8-B48F-1D18A9856A87
last_name: Stopp
- first_name: Ingrid
full_name: de Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: de Vries
- first_name: Meghan K.
full_name: Driscoll, Meghan K.
last_name: Driscoll
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Erik S.
full_name: Welf, Erik S.
last_name: Welf
- first_name: Gaudenz
full_name: Danuser, Gaudenz
last_name: Danuser
- first_name: Reto
full_name: Fiolka, Reto
last_name: Fiolka
- 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, Kopf A, Stopp JA, et al. Nuclear positioning facilitates amoeboid
migration along the path of least resistance. Nature. 2019;568:546-550.
doi:10.1038/s41586-019-1087-5
apa: Renkawitz, J., Kopf, A., Stopp, J. A., de Vries, I., Driscoll, M. K., Merrin,
J., … Sixt, M. K. (2019). Nuclear positioning facilitates amoeboid migration along
the path of least resistance. Nature. Springer Nature. https://doi.org/10.1038/s41586-019-1087-5
chicago: Renkawitz, Jörg, Aglaja Kopf, Julian A Stopp, Ingrid de Vries, Meghan K.
Driscoll, Jack Merrin, Robert Hauschild, et al. “Nuclear Positioning Facilitates
Amoeboid Migration along the Path of Least Resistance.” Nature. Springer
Nature, 2019. https://doi.org/10.1038/s41586-019-1087-5.
ieee: J. Renkawitz et al., “Nuclear positioning facilitates amoeboid migration
along the path of least resistance,” Nature, vol. 568. Springer Nature,
pp. 546–550, 2019.
ista: Renkawitz J, Kopf A, Stopp JA, de Vries I, Driscoll MK, Merrin J, Hauschild
R, Welf ES, Danuser G, Fiolka R, Sixt MK. 2019. Nuclear positioning facilitates
amoeboid migration along the path of least resistance. Nature. 568, 546–550.
mla: Renkawitz, Jörg, et al. “Nuclear Positioning Facilitates Amoeboid Migration
along the Path of Least Resistance.” Nature, vol. 568, Springer Nature,
2019, pp. 546–50, doi:10.1038/s41586-019-1087-5.
short: J. Renkawitz, A. Kopf, J.A. Stopp, I. de Vries, M.K. Driscoll, J. Merrin,
R. Hauschild, E.S. Welf, G. Danuser, R. Fiolka, M.K. Sixt, Nature 568 (2019) 546–550.
date_created: 2019-04-17T06:52:28Z
date_published: 2019-04-25T00:00:00Z
date_updated: 2026-06-05T22:32:58Z
day: '25'
department:
- _id: MiSi
- _id: NanoFab
- _id: Bio
doi: 10.1038/s41586-019-1087-5
ec_funded: 1
external_id:
isi:
- '000465594200050'
pmid:
- '30944468'
intvolume: ' 568'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217284/
month: '04'
oa: 1
oa_version: Submitted Version
page: 546-550
pmid: 1
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular Navigation Along Spatial Gradients
- _id: 265FAEBA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W01250-B20
name: Nano-Analytics of Cellular Systems
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25A48D24-B435-11E9-9278-68D0E5697425
grant_number: ALTF 1396-2014
name: Molecular and system level view of immune cell migration
publication: Nature
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/leukocytes-use-their-nucleus-as-a-ruler-to-choose-path-of-least-resistance/
record:
- id: '14697'
relation: dissertation_contains
status: public
- id: '6891'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Nuclear positioning facilitates amoeboid migration along the path of least
resistance
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 568
year: '2019'
...
---
_id: '6877'
article_processing_charge: No
article_type: original
author:
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- 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: Kopf A, Sixt MK. The neural crest pitches in to remove apoptotic debris. Cell.
2019;179(1):51-53. doi:10.1016/j.cell.2019.08.047
apa: Kopf, A., & Sixt, M. K. (2019). The neural crest pitches in to remove apoptotic
debris. Cell. Elsevier. https://doi.org/10.1016/j.cell.2019.08.047
chicago: Kopf, Aglaja, and Michael K Sixt. “The Neural Crest Pitches in to Remove
Apoptotic Debris.” Cell. Elsevier, 2019. https://doi.org/10.1016/j.cell.2019.08.047.
ieee: A. Kopf and M. K. Sixt, “The neural crest pitches in to remove apoptotic debris,”
Cell, vol. 179, no. 1. Elsevier, pp. 51–53, 2019.
ista: Kopf A, Sixt MK. 2019. The neural crest pitches in to remove apoptotic debris.
Cell. 179(1), 51–53.
mla: Kopf, Aglaja, and Michael K. Sixt. “The Neural Crest Pitches in to Remove Apoptotic
Debris.” Cell, vol. 179, no. 1, Elsevier, 2019, pp. 51–53, doi:10.1016/j.cell.2019.08.047.
short: A. Kopf, M.K. Sixt, Cell 179 (2019) 51–53.
date_created: 2019-09-15T22:00:46Z
date_published: 2019-09-19T00:00:00Z
date_updated: 2026-06-05T22:32:57Z
day: '19'
department:
- _id: MiSi
doi: 10.1016/j.cell.2019.08.047
external_id:
isi:
- '000486618500011'
pmid:
- '31539498'
intvolume: ' 179'
isi: 1
issue: '1'
language:
- iso: eng
month: '09'
oa_version: None
page: 51-53
pmid: 1
publication: Cell
publication_identifier:
eissn:
- 1097-4172
issn:
- 0092-8674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
record:
- id: '6891'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: The neural crest pitches in to remove apoptotic debris
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 179
year: '2019'
...
---
OA_place: publisher
_id: '6947'
abstract:
- lang: eng
text: Lymph nodes are es s ential organs of the immune s ys tem where adaptive
immune responses originate, and consist of various leukocyte populations and a
stromal backbone. Fibroblastic reticular cells (FRCs) are the main stromal cells
and form a sponge-like extracellular matrix network, called conduits , which they thems
elves enwrap and contract. Lymph, containing s oluble antigens , arrive
in lymph nodes via afferent lymphatic vessels that connect to the s ubcaps
ular s inus and conduit network. According to the current paradigm, the conduit network dis
tributes afferent lymph through lymph nodes and thus provides acces
s for immune cells to lymph-borne antigens. An elas tic caps ule s urrounds the organ and confines the
immune cells and FRC network. Lymph nodes are completely packed with lymphocytes and lymphocyte numbers directly dictates the
size of the organ. Although lymphocytes cons tantly enter and leave the lymph node, its s
ize remains remarkedly s table under homeostatic conditions. It is only
partly known how the cellularity and s ize of the lymph node is regulated and how the lymph node is
able to swell in inflammation. The role of the FRC network in lymph node s
welling and trans fer of fluids are inves tigated in this thes is. Furthermore, we s
tudied what trafficking routes are us ed by cancer cells in lymph nodes to form distal
metastases.We examined the role of a mechanical feedback in regulation of lymph node
swelling. Using parallel plate compression and UV-las er cutting experiments we dis
s ected the mechanical force dynamics of the whole lymph node, and individually
for FRCs and the caps ule. Physical forces generated by packed lymphocytes directly affect the tens
ion on the FRC network and capsule, which increases its resistance to swelling. This implies a feedback mechanism between tis
s ue pres s ure and ability of lymphocytes to enter the organ. Following inflammation, the lymph node swells
∼10 fold in two weeks . Yet, what is the role for tens ion on the FRC network and caps
ule, and how are lymphocytes able to enter in conditions that resist
swelling remain open ques tions . We s how that tens ion on the FRC network is important
to limit the swelling rate of the organ so that the FRC network can grow in a coordinated fashion.
This is illustrated by interfering with FRC contractility, which leads to faster
swelling rates and a dis organized FRC network in the inflamed lymph node.
Growth of the FRC network in turn is expected to releas e tens ion on thes
e s tructures and lowers the res is tance to swelling, thereby allowing
more lymphocytes to enter the organ and drive more swelling. Halt of swelling
coincides with a thickening of the caps ule, which forms a thick res
is tant band around the organ and lowers tens ion on the FRC network to form
a new force equilibrium.The FRC and conduit network are further believed to be a privileged s
ite of s oluble information within the lymph node, although many details remain uns
olved. We s how by 3D ultra-recons truction that FRCs and antigen pres
enting cells cover the s urface of conduit s ys tem for more than 99%
and we dis cus s the implications for s oluble information exchangeat the conduit
level.Finally, there is an ongoing debate in the cancer field whether and how
cancer cells in lymph nodes s eed dis tal metas tas es . We s how that cancer cells infus
ed into the lymph node can utilize trafficking routes of immune cells and rapidly migrate to blood vessels.
Once in the blood circulation, these cells are able to form metastases in
distal tissues.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
- _id: EM-Fac
alternative_title:
- ISTA Thesis
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
citation:
ama: 'Assen FP. Lymph node mechanics: Deciphering the interplay between stroma contractility,
morphology and lymphocyte trafficking. 2019. doi:10.15479/AT:ISTA:6947'
apa: 'Assen, F. P. (2019). Lymph node mechanics: Deciphering the interplay between
stroma contractility, morphology and lymphocyte trafficking. Institute of
Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:6947'
chicago: 'Assen, Frank P. “Lymph Node Mechanics: Deciphering the Interplay between
Stroma Contractility, Morphology and Lymphocyte Trafficking.” Institute of Science
and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6947.'
ieee: 'F. P. Assen, “Lymph node mechanics: Deciphering the interplay between stroma
contractility, morphology and lymphocyte trafficking,” Institute of Science and
Technology Austria, 2019.'
ista: 'Assen FP. 2019. Lymph node mechanics: Deciphering the interplay between stroma
contractility, morphology and lymphocyte trafficking. Institute of Science and
Technology Austria.'
mla: 'Assen, Frank P. Lymph Node Mechanics: Deciphering the Interplay between
Stroma Contractility, Morphology and Lymphocyte Trafficking. Institute of
Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:6947.'
short: 'F.P. Assen, Lymph Node Mechanics: Deciphering the Interplay between Stroma
Contractility, Morphology and Lymphocyte Trafficking, Institute of Science and
Technology Austria, 2019.'
corr_author: '1'
date_created: 2019-10-14T16:54:52Z
date_published: 2019-10-09T00:00:00Z
date_updated: 2026-04-08T14:01:50Z
day: '09'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:6947
file:
- access_level: closed
checksum: 53a739752a500f84d0f8ec953cbbd0b6
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: fassen
date_created: 2019-11-06T12:30:02Z
date_updated: 2020-11-07T23:30:03Z
embargo_to: open_access
file_id: '6990'
file_name: PhDthesis_FrankAssen_revised2.docx
file_size: 214172667
relation: source_file
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content_type: application/pdf
creator: fassen
date_created: 2019-11-06T12:30:57Z
date_updated: 2020-11-07T23:30:03Z
embargo: 2020-11-06
file_id: '6991'
file_name: PhDthesis_FrankAssen_revised2.pdf
file_size: 83637532
relation: main_file
file_date_updated: 2020-11-07T23:30:03Z
has_accepted_license: '1'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: '142'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '402'
relation: part_of_dissertation
status: public
- id: '664'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: 'Lymph node mechanics: Deciphering the interplay between stroma contractility,
morphology and lymphocyte trafficking'
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2019'
...
---
_id: '275'
abstract:
- lang: eng
text: Lymphatic endothelial cells (LECs) release extracellular chemokines to guide
the migration of dendritic cells. In this study, we report that LECs also release
basolateral exosome-rich endothelial vesicles (EEVs) that are secreted in greater
numbers in the presence of inflammatory cytokines and accumulate in the perivascular
stroma of small lymphatic vessels in human chronic inflammatory diseases. Proteomic
analyses of EEV fractions identified > 1,700 cargo proteins and revealed a
dominant motility-promoting protein signature. In vitro and ex vivo EEV fractions
augmented cellular protrusion formation in a CX3CL1/fractalkine-dependent fashion
and enhanced the directional migratory response of human dendritic cells along
guidance cues. We conclude that perilymphatic LEC exosomes enhance exploratory
behavior and thus promote directional migration of CX3CR1-expressing cells in
complex tissue environments.
acknowledgement: M. Brown was supported by the Cell Communication in Health and Disease
Graduate Study Program of the Austrian Science Fund and Medizinische Universität
Wien, M. Sixt by the European Research Council (ERC GA 281556) and an Austrian Science
Fund START award, K.L. Bennett by the Austrian Academy of Sciences, D.G. Jackson
and L.A. Johnson by Unit Funding (MC_UU_12010/2) and project grants from the Medical
Research Council (G1100134 and MR/L008610/1), and M. Detmar by the Schweizerischer
Nationalfonds zur Förderung der Wissenschaftlichen Forschung and Advanced European
Research Council grant LYVICAM. K. Vaahtomeri was supported by an Academy of Finland
postdoctoral research grant (287853). This project has received funding from the
European Union’s Horizon 2020 research and innovation program under grant agreement
No. 668036 (RELENT).
article_processing_charge: No
author:
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Louise
full_name: Johnson, Louise
last_name: Johnson
- first_name: Dario
full_name: Leone, Dario
last_name: Leone
- first_name: Peter
full_name: Májek, Peter
last_name: Májek
- first_name: Kari
full_name: Vaahtomeri, Kari
id: 368EE576-F248-11E8-B48F-1D18A9856A87
last_name: Vaahtomeri
orcid: 0000-0001-7829-3518
- first_name: Daniel
full_name: Senfter, Daniel
last_name: Senfter
- first_name: Nora
full_name: Bukosza, Nora
last_name: Bukosza
- first_name: Helga
full_name: Schachner, Helga
last_name: Schachner
- first_name: Gabriele
full_name: Asfour, Gabriele
last_name: Asfour
- first_name: Brigitte
full_name: Langer, Brigitte
last_name: Langer
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Katja
full_name: Parapatics, Katja
last_name: Parapatics
- first_name: Young
full_name: Hong, Young
last_name: Hong
- first_name: Keiryn
full_name: Bennett, Keiryn
last_name: Bennett
- first_name: Renate
full_name: Kain, Renate
last_name: Kain
- first_name: Michael
full_name: Detmar, Michael
last_name: Detmar
- 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: David
full_name: Jackson, David
last_name: Jackson
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
citation:
ama: Brown M, Johnson L, Leone D, et al. Lymphatic exosomes promote dendritic cell
migration along guidance cues. Journal of Cell Biology. 2018;217(6):2205-2221.
doi:10.1083/jcb.201612051
apa: Brown, M., Johnson, L., Leone, D., Májek, P., Vaahtomeri, K., Senfter, D.,
… Kerjaschki, D. (2018). Lymphatic exosomes promote dendritic cell migration along
guidance cues. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201612051
chicago: Brown, Markus, Louise Johnson, Dario Leone, Peter Májek, Kari Vaahtomeri,
Daniel Senfter, Nora Bukosza, et al. “Lymphatic Exosomes Promote Dendritic Cell
Migration along Guidance Cues.” Journal of Cell Biology. Rockefeller University
Press, 2018. https://doi.org/10.1083/jcb.201612051.
ieee: M. Brown et al., “Lymphatic exosomes promote dendritic cell migration
along guidance cues,” Journal of Cell Biology, vol. 217, no. 6. Rockefeller
University Press, pp. 2205–2221, 2018.
ista: Brown M, Johnson L, Leone D, Májek P, Vaahtomeri K, Senfter D, Bukosza N,
Schachner H, Asfour G, Langer B, Hauschild R, Parapatics K, Hong Y, Bennett K,
Kain R, Detmar M, Sixt MK, Jackson D, Kerjaschki D. 2018. Lymphatic exosomes promote
dendritic cell migration along guidance cues. Journal of Cell Biology. 217(6),
2205–2221.
mla: Brown, Markus, et al. “Lymphatic Exosomes Promote Dendritic Cell Migration
along Guidance Cues.” Journal of Cell Biology, vol. 217, no. 6, Rockefeller
University Press, 2018, pp. 2205–21, doi:10.1083/jcb.201612051.
short: M. Brown, L. Johnson, D. Leone, P. Májek, K. Vaahtomeri, D. Senfter, N. Bukosza,
H. Schachner, G. Asfour, B. Langer, R. Hauschild, K. Parapatics, Y. Hong, K. Bennett,
R. Kain, M. Detmar, M.K. Sixt, D. Jackson, D. Kerjaschki, Journal of Cell Biology
217 (2018) 2205–2221.
corr_author: '1'
date_created: 2018-12-11T11:45:33Z
date_published: 2018-04-12T00:00:00Z
date_updated: 2025-04-14T13:10:20Z
day: '12'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
doi: 10.1083/jcb.201612051
ec_funded: 1
external_id:
isi:
- '000438077800026'
pmid:
- '29650776'
file:
- access_level: open_access
checksum: 9c7eba51a35c62da8c13f98120b64df4
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T12:50:07Z
date_updated: 2020-07-14T12:45:45Z
file_id: '5704'
file_name: 2018_JournalCellBiology_Brown.pdf
file_size: 2252043
relation: main_file
file_date_updated: 2020-07-14T12:45:45Z
has_accepted_license: '1'
intvolume: ' 217'
isi: 1
issue: '6'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 2205 - 2221
pmid: 1
project:
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and force transduction of migrating leukocytes
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
publication: Journal of Cell Biology
publication_status: published
publisher: Rockefeller University Press
publist_id: '7627'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Lymphatic exosomes promote dendritic cell migration along guidance cues
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 217
year: '2018'
...
---
_id: '276'
abstract:
- lang: eng
text: Directed migration of cells relies on their ability to sense directional guidance
cues and to interact with pericellular structures in order to transduce contractile
cytoskeletal- into mechanical forces. These biomechanical processes depend highly
on microenvironmental factors such as exposure to 2D surfaces or 3D matrices.
In vivo, the majority of cells are exposed to 3D environments. Data on 3D cell
migration are mostly derived from intravital microscopy or collagen-based in vitro
assays. Both approaches offer only limited controlla-bility of experimental conditions.
Here, we developed an automated microfluidic system that allows positioning of
cells in 3D microenvironments containing highly controlled diffusion-based chemokine
gradients. Tracking migration in such gradients was feasible in real time at the
single cell level. Moreover, the setup allowed on-chip immunocytochemistry and
thus linking of functional with phenotypical properties in individual cells. Spatially
defined retrieval of cells from the device allows down-stream off-chip analysis.
Using dendritic cells as a model, our setup specifically allowed us for the first
time to quantitate key migration characteristics of cells exposed to identical
gradients of the chemokine CCL19 yet placed on 2D vs in 3D environments. Migration
properties between 2D and 3D migration were distinct. Morphological features of
cells migrating in an in vitro 3D environment were similar to those of cells migrating
in animal tissues, but different from cells migrating on a surface. Our system
thus offers a highly controllable in vitro-mimic of a 3D environment that cells
traffic in vivo.
acknowledgement: This work was supported by the Swiss National Science Foundation
(MD-PhD fellowships, 323530_164221 to C.F.; and 323630_151483 to A.J.; grant PZ00P3_144863
to M.R, grant 31003A_156431 to T.S.; PZ00P3_148000 to C.T.B.; PZ00P3_154733 to M.M.),
a Novartis “FreeNovation” grant to M.M. and T.S. and an EMBO long-term fellowship
(ALTF 1396-2014) co-funded by the European Commission (LTFCOFUND2013, GA-2013-609409)
to J.R.. M.R. was supported by the Gebert Rüf Foundation (GRS 058/14). The funders
had no role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
article_number: e0198330
article_processing_charge: No
article_type: original
author:
- first_name: Corina
full_name: Frick, Corina
last_name: Frick
- first_name: Philip
full_name: Dettinger, Philip
last_name: Dettinger
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Annaïse
full_name: Jauch, Annaïse
last_name: Jauch
- first_name: Christoph
full_name: Berger, Christoph
last_name: Berger
- first_name: Mike
full_name: Recher, Mike
last_name: Recher
- first_name: Timm
full_name: Schroeder, Timm
last_name: Schroeder
- first_name: Matthias
full_name: Mehling, Matthias
last_name: Mehling
citation:
ama: Frick C, Dettinger P, Renkawitz J, et al. Nano-scale microfluidics to study
3D chemotaxis at the single cell level. PLoS One. 2018;13(6). doi:10.1371/journal.pone.0198330
apa: Frick, C., Dettinger, P., Renkawitz, J., Jauch, A., Berger, C., Recher, M.,
… Mehling, M. (2018). Nano-scale microfluidics to study 3D chemotaxis at the single
cell level. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0198330
chicago: Frick, Corina, Philip Dettinger, Jörg Renkawitz, Annaïse Jauch, Christoph
Berger, Mike Recher, Timm Schroeder, and Matthias Mehling. “Nano-Scale Microfluidics
to Study 3D Chemotaxis at the Single Cell Level.” PLoS One. Public Library
of Science, 2018. https://doi.org/10.1371/journal.pone.0198330.
ieee: C. Frick et al., “Nano-scale microfluidics to study 3D chemotaxis at
the single cell level,” PLoS One, vol. 13, no. 6. Public Library of Science,
2018.
ista: Frick C, Dettinger P, Renkawitz J, Jauch A, Berger C, Recher M, Schroeder
T, Mehling M. 2018. Nano-scale microfluidics to study 3D chemotaxis at the single
cell level. PLoS One. 13(6), e0198330.
mla: Frick, Corina, et al. “Nano-Scale Microfluidics to Study 3D Chemotaxis at the
Single Cell Level.” PLoS One, vol. 13, no. 6, e0198330, Public Library
of Science, 2018, doi:10.1371/journal.pone.0198330.
short: C. Frick, P. Dettinger, J. Renkawitz, A. Jauch, C. Berger, M. Recher, T.
Schroeder, M. Mehling, PLoS One 13 (2018).
date_created: 2018-12-11T11:45:34Z
date_published: 2018-06-07T00:00:00Z
date_updated: 2023-09-13T09:00:15Z
day: '07'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1371/journal.pone.0198330
external_id:
isi:
- '000434384900031'
file:
- access_level: open_access
checksum: 95fc5dc3938b3ad3b7697d10c83cc143
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T14:10:32Z
date_updated: 2020-07-14T12:45:45Z
file_id: '5709'
file_name: 2018_Plos_Frick.pdf
file_size: 7682167
relation: main_file
file_date_updated: 2020-07-14T12:45:45Z
has_accepted_license: '1'
intvolume: ' 13'
isi: 1
issue: '6'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '7626'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nano-scale microfluidics to study 3D chemotaxis at the single cell level
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 13
year: '2018'
...
---
_id: '308'
abstract:
- lang: eng
text: Migrating cells penetrate tissue barriers during development, inflammatory
responses, and tumor metastasis. We study if migration in vivo in such three-dimensionally
confined environments requires changes in the mechanical properties of the surrounding
cells using embryonic Drosophila melanogaster hemocytes, also called macrophages,
as a model. We find that macrophage invasion into the germband through transient
separation of the apposing ectoderm and mesoderm requires cell deformations and
reductions in apical tension in the ectoderm. Interestingly, the genetic pathway
governing these mechanical shifts acts downstream of the only known tumor necrosis
factor superfamily member in Drosophila, Eiger, and its receptor, Grindelwald.
Eiger-Grindelwald signaling reduces levels of active Myosin in the germband ectodermal
cortex through the localization of a Crumbs complex component, Patj (Pals-1-associated
tight junction protein). We therefore elucidate a distinct molecular pathway that
controls tissue tension and demonstrate the importance of such regulation for
invasive migration in vivo.
acknowledged_ssus:
- _id: SSU
article_processing_charge: No
article_type: original
author:
- first_name: Aparna
full_name: Ratheesh, Aparna
id: 2F064CFE-F248-11E8-B48F-1D18A9856A87
last_name: Ratheesh
orcid: 0000-0001-7190-0776
- first_name: Julia
full_name: Biebl, Julia
id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87
last_name: Biebl
- first_name: Michael
full_name: Smutny, Michael
last_name: Smutny
- first_name: Jana
full_name: Veselá, Jana
id: 433253EE-F248-11E8-B48F-1D18A9856A87
last_name: Veselá
- first_name: Ekaterina
full_name: Papusheva, Ekaterina
id: 41DB591E-F248-11E8-B48F-1D18A9856A87
last_name: Papusheva
- first_name: Gabriel
full_name: Krens, Gabriel
id: 2B819732-F248-11E8-B48F-1D18A9856A87
last_name: Krens
orcid: 0000-0003-4761-5996
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Attila
full_name: György, Attila
id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87
last_name: György
orcid: 0000-0002-1819-198X
- first_name: Alessandra M
full_name: Casano, Alessandra M
id: 3DBA3F4E-F248-11E8-B48F-1D18A9856A87
last_name: Casano
orcid: 0000-0002-6009-6804
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
citation:
ama: Ratheesh A, Bicher J, Smutny M, et al. Drosophila TNF modulates tissue tension
in the embryo to facilitate macrophage invasive migration. Developmental Cell.
2018;45(3):331-346. doi:10.1016/j.devcel.2018.04.002
apa: Ratheesh, A., Bicher, J., Smutny, M., Veselá, J., Papusheva, E., Krens, G.,
… Siekhaus, D. E. (2018). Drosophila TNF modulates tissue tension in the embryo
to facilitate macrophage invasive migration. Developmental Cell. Elsevier.
https://doi.org/10.1016/j.devcel.2018.04.002
chicago: Ratheesh, Aparna, Julia Bicher, Michael Smutny, Jana Veselá, Ekaterina
Papusheva, Gabriel Krens, Walter Kaufmann, Attila György, Alessandra M Casano,
and Daria E Siekhaus. “Drosophila TNF Modulates Tissue Tension in the Embryo to
Facilitate Macrophage Invasive Migration.” Developmental Cell. Elsevier,
2018. https://doi.org/10.1016/j.devcel.2018.04.002.
ieee: A. Ratheesh et al., “Drosophila TNF modulates tissue tension in the
embryo to facilitate macrophage invasive migration,” Developmental Cell,
vol. 45, no. 3. Elsevier, pp. 331–346, 2018.
ista: Ratheesh A, Bicher J, Smutny M, Veselá J, Papusheva E, Krens G, Kaufmann W,
György A, Casano AM, Siekhaus DE. 2018. Drosophila TNF modulates tissue tension
in the embryo to facilitate macrophage invasive migration. Developmental Cell.
45(3), 331–346.
mla: Ratheesh, Aparna, et al. “Drosophila TNF Modulates Tissue Tension in the Embryo
to Facilitate Macrophage Invasive Migration.” Developmental Cell, vol.
45, no. 3, Elsevier, 2018, pp. 331–46, doi:10.1016/j.devcel.2018.04.002.
short: A. Ratheesh, J. Bicher, M. Smutny, J. Veselá, E. Papusheva, G. Krens, W.
Kaufmann, A. György, A.M. Casano, D.E. Siekhaus, Developmental Cell 45 (2018)
331–346.
corr_author: '1'
date_created: 2018-12-11T11:45:44Z
date_published: 2018-05-07T00:00:00Z
date_updated: 2024-10-22T10:12:36Z
day: '07'
department:
- _id: DaSi
- _id: CaHe
- _id: Bio
- _id: EM-Fac
- _id: MiSi
doi: 10.1016/j.devcel.2018.04.002
ec_funded: 1
external_id:
isi:
- '000432461400009'
pmid:
- '29738712'
intvolume: ' 45'
isi: 1
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.devcel.2018.04.002
month: '05'
oa: 1
oa_version: Published Version
page: 331 - 346
pmid: 1
project:
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P29638
name: The role of Drosophila TNF alpha in immune cell invasion
- _id: 2536F660-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
publication: Developmental Cell
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/cells-change-tension-to-make-tissue-barriers-easier-to-get-through/
scopus_import: '1'
status: public
title: Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage
invasive migration
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 45
year: '2018'
...
---
_id: '318'
abstract:
- lang: eng
text: The insect’s fat body combines metabolic and immunological functions. In this
issue of Developmental Cell, Franz et al. (2018) show that in Drosophila, cells
of the fat body are not static, but can actively “swim” toward sites of epithelial
injury, where they physically clog the wound and locally secrete antimicrobial
peptides.
acknowledgement: Short Survey
article_processing_charge: No
author:
- first_name: Alessandra M
full_name: Casano, Alessandra M
id: 3DBA3F4E-F248-11E8-B48F-1D18A9856A87
last_name: Casano
orcid: 0000-0002-6009-6804
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Casano AM, Sixt MK. A fat lot of good for wound healing. Developmental Cell.
2018;44(4):405-406. doi:10.1016/j.devcel.2018.02.009
apa: Casano, A. M., & Sixt, M. K. (2018). A fat lot of good for wound healing.
Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2018.02.009
chicago: Casano, Alessandra M, and Michael K Sixt. “A Fat Lot of Good for Wound
Healing.” Developmental Cell. Cell Press, 2018. https://doi.org/10.1016/j.devcel.2018.02.009.
ieee: A. M. Casano and M. K. Sixt, “A fat lot of good for wound healing,” Developmental
Cell, vol. 44, no. 4. Cell Press, pp. 405–406, 2018.
ista: Casano AM, Sixt MK. 2018. A fat lot of good for wound healing. Developmental
Cell. 44(4), 405–406.
mla: Casano, Alessandra M., and Michael K. Sixt. “A Fat Lot of Good for Wound Healing.”
Developmental Cell, vol. 44, no. 4, Cell Press, 2018, pp. 405–06, doi:10.1016/j.devcel.2018.02.009.
short: A.M. Casano, M.K. Sixt, Developmental Cell 44 (2018) 405–406.
corr_author: '1'
date_created: 2018-12-11T11:45:47Z
date_published: 2018-02-26T00:00:00Z
date_updated: 2024-10-09T20:58:17Z
day: '26'
department:
- _id: MiSi
doi: 10.1016/j.devcel.2018.02.009
external_id:
isi:
- '000426150700002'
pmid:
- '29486189'
intvolume: ' 44'
isi: 1
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/29486189
month: '02'
oa: 1
oa_version: Published Version
page: 405 - 406
pmid: 1
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '7547'
quality_controlled: '1'
scopus_import: '1'
status: public
title: A fat lot of good for wound healing
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 44
year: '2018'
...
---
_id: '153'
abstract:
- lang: eng
text: Cells migrating in multicellular organisms steadily traverse complex three-dimensional
(3D) environments. To decipher the underlying cell biology, current experimental
setups either use simplified 2D, tissue-mimetic 3D (e.g., collagen matrices) or
in vivo environments. While only in vivo experiments are truly physiological,
they do not allow for precise manipulation of environmental parameters. 2D in
vitro experiments do allow mechanical and chemical manipulations, but increasing
evidence demonstrates substantial differences of migratory mechanisms in 2D and
3D. Here, we describe simple, robust, and versatile “pillar forests” to investigate
cell migration in complex but fully controllable 3D environments. Pillar forests
are polydimethylsiloxane-based setups, in which two closely adjacent surfaces
are interconnected by arrays of micrometer-sized pillars. Changing the pillar
shape, size, height and the inter-pillar distance precisely manipulates microenvironmental
parameters (e.g., pore sizes, micro-geometry, micro-topology), while being easily
combined with chemotactic cues, surface coatings, diverse cell types and advanced
imaging techniques. Thus, pillar forests combine the advantages of 2D cell migration
assays with the precise definition of 3D environmental parameters.
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: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- 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: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- 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, Reversat A, Leithner AF, Merrin J, Sixt MK. Micro-engineered
“pillar forests” to study cell migration in complex but controlled 3D environments.
In: Methods in Cell Biology. Vol 147. Academic Press; 2018:79-91. doi:10.1016/bs.mcb.2018.07.004'
apa: Renkawitz, J., Reversat, A., Leithner, A. F., Merrin, J., & Sixt, M. K.
(2018). Micro-engineered “pillar forests” to study cell migration in complex but
controlled 3D environments. In Methods in Cell Biology (Vol. 147, pp. 79–91).
Academic Press. https://doi.org/10.1016/bs.mcb.2018.07.004
chicago: Renkawitz, Jörg, Anne Reversat, Alexander F Leithner, Jack Merrin, and
Michael K Sixt. “Micro-Engineered ‘Pillar Forests’ to Study Cell Migration in
Complex but Controlled 3D Environments.” In Methods in Cell Biology, 147:79–91.
Academic Press, 2018. https://doi.org/10.1016/bs.mcb.2018.07.004.
ieee: J. Renkawitz, A. Reversat, A. F. Leithner, J. Merrin, and M. K. Sixt, “Micro-engineered
‘pillar forests’ to study cell migration in complex but controlled 3D environments,”
in Methods in Cell Biology, vol. 147, Academic Press, 2018, pp. 79–91.
ista: 'Renkawitz J, Reversat A, Leithner AF, Merrin J, Sixt MK. 2018.Micro-engineered
“pillar forests” to study cell migration in complex but controlled 3D environments.
In: Methods in Cell Biology. vol. 147, 79–91.'
mla: Renkawitz, Jörg, et al. “Micro-Engineered ‘Pillar Forests’ to Study Cell Migration
in Complex but Controlled 3D Environments.” Methods in Cell Biology, vol.
147, Academic Press, 2018, pp. 79–91, doi:10.1016/bs.mcb.2018.07.004.
short: J. Renkawitz, A. Reversat, A.F. Leithner, J. Merrin, M.K. Sixt, in:, Methods
in Cell Biology, Academic Press, 2018, pp. 79–91.
date_created: 2018-12-11T11:44:54Z
date_published: 2018-07-27T00:00:00Z
date_updated: 2025-07-10T11:51:09Z
day: '27'
department:
- _id: MiSi
- _id: NanoFab
doi: 10.1016/bs.mcb.2018.07.004
external_id:
isi:
- '000452412300006'
pmid:
- '30165964'
intvolume: ' 147'
isi: 1
language:
- iso: eng
month: '07'
oa_version: None
page: 79 - 91
pmid: 1
publication: Methods in Cell Biology
publication_identifier:
issn:
- 0091-679X
publication_status: published
publisher: Academic Press
publist_id: '7768'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Micro-engineered “pillar forests” to study cell migration in complex but controlled
3D environments
type: book_chapter
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 147
year: '2018'
...
---
_id: '5858'
abstract:
- lang: eng
text: Spatial patterns are ubiquitous on the subcellular, cellular and tissue level,
and can be studied using imaging techniques such as light and fluorescence microscopy.
Imaging data provide quantitative information about biological systems; however,
mechanisms causing spatial patterning often remain elusive. In recent years, spatio-temporal
mathematical modelling has helped to overcome this problem. Yet, outliers and
structured noise limit modelling of whole imaging data, and models often consider
spatial summary statistics. Here, we introduce an integrated data-driven modelling
approach that can cope with measurement artefacts and whole imaging data. Our
approach combines mechanistic models of the biological processes with robust statistical
models of the measurement process. The parameters of the integrated model are
calibrated using a maximum-likelihood approach. We used this integrated modelling
approach to study in vivo gradients of the chemokine (C-C motif) ligand 21 (CCL21).
CCL21 gradients guide dendritic cells and are important in the adaptive immune
response. Using artificial data, we verified that the integrated modelling approach
provides reliable parameter estimates in the presence of measurement noise and
that bias and variance of these estimates are reduced compared to conventional
approaches. The application to experimental data allowed the parametrization and
subsequent refinement of the model using additional mechanisms. Among other results,
model-based hypothesis testing predicted lymphatic vessel-dependent concentration
of heparan sulfate, the binding partner of CCL21. The selected model provided
an accurate description of the experimental data and was partially validated using
published data. Our findings demonstrate that integrated statistical modelling
of whole imaging data is computationally feasible and can provide novel biological
insights.
article_number: '20180600'
article_processing_charge: No
author:
- first_name: Sabrina
full_name: Hross, Sabrina
last_name: Hross
- first_name: Fabian J.
full_name: Theis, Fabian J.
last_name: Theis
- 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: Jan
full_name: Hasenauer, Jan
last_name: Hasenauer
citation:
ama: Hross S, Theis FJ, Sixt MK, Hasenauer J. Mechanistic description of spatial
processes using integrative modelling of noise-corrupted imaging data. Journal
of the Royal Society Interface. 2018;15(149). doi:10.1098/rsif.2018.0600
apa: Hross, S., Theis, F. J., Sixt, M. K., & Hasenauer, J. (2018). Mechanistic
description of spatial processes using integrative modelling of noise-corrupted
imaging data. Journal of the Royal Society Interface. Royal Society Publishing.
https://doi.org/10.1098/rsif.2018.0600
chicago: Hross, Sabrina, Fabian J. Theis, Michael K Sixt, and Jan Hasenauer. “Mechanistic
Description of Spatial Processes Using Integrative Modelling of Noise-Corrupted
Imaging Data.” Journal of the Royal Society Interface. Royal Society Publishing,
2018. https://doi.org/10.1098/rsif.2018.0600.
ieee: S. Hross, F. J. Theis, M. K. Sixt, and J. Hasenauer, “Mechanistic description
of spatial processes using integrative modelling of noise-corrupted imaging data,”
Journal of the Royal Society Interface, vol. 15, no. 149. Royal Society
Publishing, 2018.
ista: Hross S, Theis FJ, Sixt MK, Hasenauer J. 2018. Mechanistic description of
spatial processes using integrative modelling of noise-corrupted imaging data.
Journal of the Royal Society Interface. 15(149), 20180600.
mla: Hross, Sabrina, et al. “Mechanistic Description of Spatial Processes Using
Integrative Modelling of Noise-Corrupted Imaging Data.” Journal of the Royal
Society Interface, vol. 15, no. 149, 20180600, Royal Society Publishing, 2018,
doi:10.1098/rsif.2018.0600.
short: S. Hross, F.J. Theis, M.K. Sixt, J. Hasenauer, Journal of the Royal Society
Interface 15 (2018).
date_created: 2019-01-20T22:59:18Z
date_published: 2018-12-05T00:00:00Z
date_updated: 2025-07-10T11:53:04Z
day: '05'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1098/rsif.2018.0600
external_id:
isi:
- '000456783800011'
file:
- access_level: open_access
checksum: 56eb4308a15b7190bff938fab1f780e8
content_type: application/pdf
creator: dernst
date_created: 2019-02-05T14:46:44Z
date_updated: 2020-07-14T12:47:13Z
file_id: '5925'
file_name: 2018_Interface_Hross.pdf
file_size: 1464288
relation: main_file
file_date_updated: 2020-07-14T12:47:13Z
has_accepted_license: '1'
intvolume: ' 15'
isi: 1
issue: '149'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
publication: Journal of the Royal Society Interface
publication_identifier:
issn:
- 1742-5689
publication_status: published
publisher: Royal Society Publishing
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mechanistic description of spatial processes using integrative modelling of
noise-corrupted imaging data
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 15
year: '2018'
...
---
_id: '5861'
abstract:
- lang: eng
text: In zebrafish larvae, it is the cell type that determines how the cell responds
to a chemokine signal.
article_number: e37888
article_processing_charge: No
article_type: original
author:
- first_name: Jonna H
full_name: Alanko, Jonna H
id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87
last_name: Alanko
orcid: 0000-0002-7698-3061
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Alanko JH, Sixt MK. The cell sets the tone. eLife. 2018;7. doi:10.7554/eLife.37888
apa: Alanko, J. H., & Sixt, M. K. (2018). The cell sets the tone. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.37888
chicago: Alanko, Jonna H, and Michael K Sixt. “The Cell Sets the Tone.” ELife.
eLife Sciences Publications, 2018. https://doi.org/10.7554/eLife.37888.
ieee: J. H. Alanko and M. K. Sixt, “The cell sets the tone,” eLife, vol.
7. eLife Sciences Publications, 2018.
ista: Alanko JH, Sixt MK. 2018. The cell sets the tone. eLife. 7, e37888.
mla: Alanko, Jonna H., and Michael K. Sixt. “The Cell Sets the Tone.” ELife,
vol. 7, e37888, eLife Sciences Publications, 2018, doi:10.7554/eLife.37888.
short: J.H. Alanko, M.K. Sixt, ELife 7 (2018).
corr_author: '1'
date_created: 2019-01-20T22:59:19Z
date_published: 2018-06-06T00:00:00Z
date_updated: 2025-07-10T11:53:05Z
day: '06'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.7554/eLife.37888
external_id:
isi:
- '000434375000001'
file:
- access_level: open_access
checksum: f1c7ec2a809408d763c4b529a98f9a3b
content_type: application/pdf
creator: dernst
date_created: 2019-02-13T10:52:11Z
date_updated: 2020-07-14T12:47:13Z
file_id: '5973'
file_name: 2018_eLife_Alanko.pdf
file_size: 358141
relation: main_file
file_date_updated: 2020-07-14T12:47:13Z
has_accepted_license: '1'
intvolume: ' 7'
isi: 1
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: The cell sets the tone
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 7
year: '2018'
...
---
_id: '5984'
abstract:
- lang: eng
text: G-protein-coupled receptors (GPCRs) form the largest receptor family, relay
environmental stimuli to changes in cell behavior and represent prime drug targets.
Many GPCRs are classified as orphan receptors because of the limited knowledge
on their ligands and coupling to cellular signaling machineries. Here, we engineer
a library of 63 chimeric receptors that contain the signaling domains of human
orphan and understudied GPCRs functionally linked to the light-sensing domain
of rhodopsin. Upon stimulation with visible light, we identify activation of canonical
cell signaling pathways, including cAMP-, Ca2+-, MAPK/ERK-, and Rho-dependent
pathways, downstream of the engineered receptors. For the human pseudogene GPR33,
we resurrect a signaling function that supports its hypothesized role as a pathogen
entry site. These results demonstrate that substituting unknown chemical activators
with a light switch can reveal information about protein function and provide
an optically controlled protein library for exploring the physiology and therapeutic
potential of understudied GPCRs.
article_number: '1950'
article_processing_charge: No
author:
- first_name: Maurizio
full_name: Morri, Maurizio
id: 4863116E-F248-11E8-B48F-1D18A9856A87
last_name: Morri
- first_name: Inmaculada
full_name: Sanchez-Romero, Inmaculada
id: 3D9C5D30-F248-11E8-B48F-1D18A9856A87
last_name: Sanchez-Romero
- first_name: Alexandra-Madelaine
full_name: Tichy, Alexandra-Madelaine
id: 29D8BB2C-F248-11E8-B48F-1D18A9856A87
last_name: Tichy
- first_name: Stephanie
full_name: Kainrath, Stephanie
id: 32CFBA64-F248-11E8-B48F-1D18A9856A87
last_name: Kainrath
- first_name: Elliot J.
full_name: Gerrard, Elliot J.
last_name: Gerrard
- first_name: Priscila
full_name: Hirschfeld, Priscila
id: 435ACB3A-F248-11E8-B48F-1D18A9856A87
last_name: Hirschfeld
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Harald L
full_name: Janovjak, Harald L
id: 33BA6C30-F248-11E8-B48F-1D18A9856A87
last_name: Janovjak
orcid: 0000-0002-8023-9315
citation:
ama: Morri M, Sanchez-Romero I, Tichy A-M, et al. Optical functionalization of human
class A orphan G-protein-coupled receptors. Nature Communications. 2018;9(1).
doi:10.1038/s41467-018-04342-1
apa: Morri, M., Sanchez-Romero, I., Tichy, A.-M., Kainrath, S., Gerrard, E. J.,
Hirschfeld, P., … Janovjak, H. L. (2018). Optical functionalization of human class
A orphan G-protein-coupled receptors. Nature Communications. Springer Nature.
https://doi.org/10.1038/s41467-018-04342-1
chicago: Morri, Maurizio, Inmaculada Sanchez-Romero, Alexandra-Madelaine Tichy,
Stephanie Kainrath, Elliot J. Gerrard, Priscila Hirschfeld, Jan Schwarz, and Harald
L Janovjak. “Optical Functionalization of Human Class A Orphan G-Protein-Coupled
Receptors.” Nature Communications. Springer Nature, 2018. https://doi.org/10.1038/s41467-018-04342-1.
ieee: M. Morri et al., “Optical functionalization of human class A orphan
G-protein-coupled receptors,” Nature Communications, vol. 9, no. 1. Springer
Nature, 2018.
ista: Morri M, Sanchez-Romero I, Tichy A-M, Kainrath S, Gerrard EJ, Hirschfeld P,
Schwarz J, Janovjak HL. 2018. Optical functionalization of human class A orphan
G-protein-coupled receptors. Nature Communications. 9(1), 1950.
mla: Morri, Maurizio, et al. “Optical Functionalization of Human Class A Orphan
G-Protein-Coupled Receptors.” Nature Communications, vol. 9, no. 1, 1950,
Springer Nature, 2018, doi:10.1038/s41467-018-04342-1.
short: M. Morri, I. Sanchez-Romero, A.-M. Tichy, S. Kainrath, E.J. Gerrard, P. Hirschfeld,
J. Schwarz, H.L. Janovjak, Nature Communications 9 (2018).
date_created: 2019-02-14T10:50:24Z
date_published: 2018-12-01T00:00:00Z
date_updated: 2025-04-15T07:22:42Z
day: '01'
ddc:
- '570'
department:
- _id: HaJa
- _id: CaGu
- _id: MiSi
doi: 10.1038/s41467-018-04342-1
ec_funded: 1
external_id:
isi:
- '000432280000006'
file:
- access_level: open_access
checksum: 8325fcc194264af4749e662a73bf66b5
content_type: application/pdf
creator: kschuh
date_created: 2019-02-14T10:58:29Z
date_updated: 2020-07-14T12:47:14Z
file_id: '5985'
file_name: 2018_Springer_Morri.pdf
file_size: 1349914
relation: main_file
file_date_updated: 2020-07-14T12:47:14Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
issue: '1'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 25548C20-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '303564'
name: Microbial Ion Channels for Synthetic Neurobiology
- _id: 255A6082-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W1232-B24
name: Molecular Drug Targets
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Optical functionalization of human class A orphan G-protein-coupled receptors
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 9
year: '2018'
...
---
_id: '5992'
abstract:
- lang: eng
text: Lamellipodia are flat membrane protrusions formed during mesenchymal motion.
Polymerization at the leading edge assembles the actin filament network and generates
protrusion force. How this force is supported by the network and how the assembly
rate is shared between protrusion and network retrograde flow determines the protrusion
rate. We use mathematical modeling to understand experiments changing the F-actin
density in lamellipodia of B16-F1 melanoma cells by modulation of Arp2/3 complex
activity or knockout of the formins FMNL2 and FMNL3. Cells respond to a reduction
of density with a decrease of protrusion velocity, an increase in the ratio of
force to filament number, but constant network assembly rate. The relation between
protrusion force and tension gradient in the F-actin network and the density dependency
of friction, elasticity, and viscosity of the network explain the experimental
observations. The formins act as filament nucleators and elongators with differential
rates. Modulation of their activity suggests an effect on network assembly rate.
Contrary to these expectations, the effect of changes in elongator composition
is much weaker than the consequences of the density change. We conclude that the
force acting on the leading edge membrane is the force required to drive F-actin
network retrograde flow.
article_processing_charge: No
author:
- first_name: Setareh
full_name: Dolati, Setareh
last_name: Dolati
- first_name: Frieda
full_name: Kage, Frieda
last_name: Kage
- first_name: Jan
full_name: Mueller, Jan
last_name: Mueller
- first_name: Mathias
full_name: Müsken, Mathias
last_name: Müsken
- first_name: Marieluise
full_name: Kirchner, Marieluise
last_name: Kirchner
- first_name: Gunnar
full_name: Dittmar, Gunnar
last_name: Dittmar
- 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: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Martin
full_name: Falcke, Martin
last_name: Falcke
citation:
ama: Dolati S, Kage F, Mueller J, et al. On the relation between filament density,
force generation, and protrusion rate in mesenchymal cell motility. Molecular
Biology of the Cell. 2018;29(22):2674-2686. doi:10.1091/mbc.e18-02-0082
apa: Dolati, S., Kage, F., Mueller, J., Müsken, M., Kirchner, M., Dittmar, G., …
Falcke, M. (2018). On the relation between filament density, force generation,
and protrusion rate in mesenchymal cell motility. Molecular Biology of the
Cell. American Society for Cell Biology . https://doi.org/10.1091/mbc.e18-02-0082
chicago: Dolati, Setareh, Frieda Kage, Jan Mueller, Mathias Müsken, Marieluise Kirchner,
Gunnar Dittmar, Michael K Sixt, Klemens Rottner, and Martin Falcke. “On the Relation
between Filament Density, Force Generation, and Protrusion Rate in Mesenchymal
Cell Motility.” Molecular Biology of the Cell. American Society for Cell
Biology , 2018. https://doi.org/10.1091/mbc.e18-02-0082.
ieee: S. Dolati et al., “On the relation between filament density, force
generation, and protrusion rate in mesenchymal cell motility,” Molecular Biology
of the Cell, vol. 29, no. 22. American Society for Cell Biology , pp. 2674–2686,
2018.
ista: Dolati S, Kage F, Mueller J, Müsken M, Kirchner M, Dittmar G, Sixt MK, Rottner
K, Falcke M. 2018. On the relation between filament density, force generation,
and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell.
29(22), 2674–2686.
mla: Dolati, Setareh, et al. “On the Relation between Filament Density, Force Generation,
and Protrusion Rate in Mesenchymal Cell Motility.” Molecular Biology of the
Cell, vol. 29, no. 22, American Society for Cell Biology , 2018, pp. 2674–86,
doi:10.1091/mbc.e18-02-0082.
short: S. Dolati, F. Kage, J. Mueller, M. Müsken, M. Kirchner, G. Dittmar, M.K.
Sixt, K. Rottner, M. Falcke, Molecular Biology of the Cell 29 (2018) 2674–2686.
date_created: 2019-02-14T12:25:47Z
date_published: 2018-11-01T00:00:00Z
date_updated: 2023-09-19T14:30:23Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1091/mbc.e18-02-0082
external_id:
isi:
- '000455641000011'
pmid:
- '30156465'
file:
- access_level: open_access
checksum: e98465b4416b3e804c47f40086932af2
content_type: application/pdf
creator: kschuh
date_created: 2019-02-14T12:34:29Z
date_updated: 2020-07-14T12:47:15Z
file_id: '5994'
file_name: 2018_ASCB_Dolati.pdf
file_size: 6668971
relation: main_file
file_date_updated: 2020-07-14T12:47:15Z
has_accepted_license: '1'
intvolume: ' 29'
isi: 1
issue: '22'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-sa/4.0/
month: '11'
oa: 1
oa_version: Published Version
page: 2674-2686
pmid: 1
publication: Molecular Biology of the Cell
publication_identifier:
eissn:
- 1939-4586
publication_status: published
publisher: 'American Society for Cell Biology '
quality_controlled: '1'
scopus_import: '1'
status: public
title: On the relation between filament density, force generation, and protrusion
rate in mesenchymal cell motility
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 29
year: '2018'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '6354'
abstract:
- lang: eng
text: Blood platelets are critical for hemostasis and thrombosis, but also play
diverse roles during immune responses. We have recently reported that platelets
migrate at sites of infection in vitro and in vivo. Importantly, platelets use
their ability to migrate to collect and bundle fibrin (ogen)-bound bacteria accomplishing
efficient intravascular bacterial trapping. Here, we describe a method that allows
analyzing platelet migration in vitro, focusing on their ability to collect bacteria
and trap bacteria under flow.
acknowledgement: This protocol was adapted from a previously published study (Gaertner
et al., 2017). We thank Michael Lorenz for his excellent assistance in bacteria
culture. This work was funded by the DFG SFB 914 (S.M. [B02 and Z01]), the DFG SFB
1123 (S.M. [B06]), the DFG FOR 2033 (S.M. and F.G.), the German Centre for Cardiovascular
Research (DZHK) (MHA 1.4VD [S.M.]), FP7 program (project 260309, PRESTIGE [S.M.]),
FöFoLe project 947 (F.G.), the Friedrich-Baur-Stiftung project 41/16 (F.G.), Marie
Sklodowska Curie Individual Fellowship (EU project 747687, LamelliaActin [F.G.]).
article_number: e3018
article_processing_charge: Yes
article_type: original
author:
- first_name: Shuxia
full_name: Fan, Shuxia
last_name: Fan
- first_name: Michael
full_name: Lorenz, Michael
last_name: Lorenz
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
citation:
ama: Fan S, Lorenz M, Massberg S, Gärtner FR. Platelet migration and bacterial trapping
assay under flow. Bio-Protocol. 2018;8(18). doi:10.21769/bioprotoc.3018
apa: Fan, S., Lorenz, M., Massberg, S., & Gärtner, F. R. (2018). Platelet migration
and bacterial trapping assay under flow. Bio-Protocol. Bio-Protocol. https://doi.org/10.21769/bioprotoc.3018
chicago: Fan, Shuxia, Michael Lorenz, Steffen Massberg, and Florian R Gärtner. “Platelet
Migration and Bacterial Trapping Assay under Flow.” Bio-Protocol. Bio-Protocol,
2018. https://doi.org/10.21769/bioprotoc.3018.
ieee: S. Fan, M. Lorenz, S. Massberg, and F. R. Gärtner, “Platelet migration and
bacterial trapping assay under flow,” Bio-Protocol, vol. 8, no. 18. Bio-Protocol,
2018.
ista: Fan S, Lorenz M, Massberg S, Gärtner FR. 2018. Platelet migration and bacterial
trapping assay under flow. Bio-Protocol. 8(18), e3018.
mla: Fan, Shuxia, et al. “Platelet Migration and Bacterial Trapping Assay under
Flow.” Bio-Protocol, vol. 8, no. 18, e3018, Bio-Protocol, 2018, doi:10.21769/bioprotoc.3018.
short: S. Fan, M. Lorenz, S. Massberg, F.R. Gärtner, Bio-Protocol 8 (2018).
corr_author: '1'
date_created: 2019-04-29T09:40:33Z
date_published: 2018-09-20T00:00:00Z
date_updated: 2025-05-20T07:43:06Z
day: '20'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.21769/bioprotoc.3018
ec_funded: 1
external_id:
pmid:
- '34395806'
file:
- access_level: open_access
checksum: d4588377e789da7f360b553ae02c5119
content_type: application/pdf
creator: dernst
date_created: 2019-04-30T08:04:33Z
date_updated: 2020-07-14T12:47:28Z
file_id: '6360'
file_name: 2018_BioProtocol_Fan.pdf
file_size: 2928337
relation: main_file
file_date_updated: 2020-07-14T12:47:28Z
has_accepted_license: '1'
intvolume: ' 8'
issue: '18'
keyword:
- Platelets
- Cell migration
- Bacteria
- Shear flow
- Fibrinogen
- E. coli
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Bio-Protocol
publication_identifier:
issn:
- 2331-8325
publication_status: published
publisher: Bio-Protocol
quality_controlled: '1'
status: public
title: Platelet migration and bacterial trapping assay under flow
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2018'
...
---
_id: '6497'
abstract:
- lang: eng
text: T cells are actively scanning pMHC-presenting cells in lymphoid organs and
nonlymphoid tissues (NLTs) with divergent topologies and confinement. How the
T cell actomyosin cytoskeleton facilitates this task in distinct environments
is incompletely understood. Here, we show that lack of Myosin IXb (Myo9b), a negative
regulator of the small GTPase Rho, led to increased Rho-GTP levels and cell surface
stiffness in primary T cells. Nonetheless, intravital imaging revealed robust
motility of Myo9b−/− CD8+ T cells in lymphoid tissue and similar expansion and
differentiation during immune responses. In contrast, accumulation of Myo9b−/−
CD8+ T cells in NLTs was strongly impaired. Specifically, Myo9b was required for
T cell crossing of basement membranes, such as those which are present between
dermis and epidermis. As consequence, Myo9b−/− CD8+ T cells showed impaired control
of skin infections. In sum, we show that Myo9b is critical for the CD8+ T cell
adaptation from lymphoid to NLT surveillance and the establishment of protective
tissue–resident T cell populations.
article_processing_charge: No
author:
- first_name: Federica
full_name: Moalli, Federica
last_name: Moalli
- first_name: Xenia
full_name: Ficht, Xenia
last_name: Ficht
- first_name: Philipp
full_name: Germann, Philipp
last_name: Germann
- first_name: Mykhailo
full_name: Vladymyrov, Mykhailo
last_name: Vladymyrov
- first_name: Bettina
full_name: Stolp, Bettina
last_name: Stolp
- first_name: Ingrid
full_name: de Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: de Vries
- first_name: Ruth
full_name: Lyck, Ruth
last_name: Lyck
- first_name: Jasmin
full_name: Balmer, Jasmin
last_name: Balmer
- first_name: Amleto
full_name: Fiocchi, Amleto
last_name: Fiocchi
- first_name: Mario
full_name: Kreutzfeldt, Mario
last_name: Kreutzfeldt
- first_name: Doron
full_name: Merkler, Doron
last_name: Merkler
- first_name: Matteo
full_name: Iannacone, Matteo
last_name: Iannacone
- first_name: Akitaka
full_name: Ariga, Akitaka
last_name: Ariga
- first_name: Michael H.
full_name: Stoffel, Michael H.
last_name: Stoffel
- first_name: James
full_name: Sharpe, James
last_name: Sharpe
- first_name: Martin
full_name: Bähler, Martin
last_name: Bähler
- 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: Alba
full_name: Diz-Muñoz, Alba
last_name: Diz-Muñoz
- first_name: Jens V.
full_name: Stein, Jens V.
last_name: Stein
citation:
ama: Moalli F, Ficht X, Germann P, et al. The Rho regulator Myosin IXb enables nonlymphoid
tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine.
2018;2015(7):1869–1890. doi:10.1084/jem.20170896
apa: Moalli, F., Ficht, X., Germann, P., Vladymyrov, M., Stolp, B., de Vries, I.,
… Stein, J. V. (2018). The Rho regulator Myosin IXb enables nonlymphoid tissue
seeding of protective CD8+T cells. The Journal of Experimental Medicine.
Rockefeller University Press. https://doi.org/10.1084/jem.20170896
chicago: Moalli, Federica, Xenia Ficht, Philipp Germann, Mykhailo Vladymyrov, Bettina
Stolp, Ingrid de Vries, Ruth Lyck, et al. “The Rho Regulator Myosin IXb Enables
Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” The Journal of Experimental
Medicine. Rockefeller University Press, 2018. https://doi.org/10.1084/jem.20170896.
ieee: F. Moalli et al., “The Rho regulator Myosin IXb enables nonlymphoid
tissue seeding of protective CD8+T cells,” The Journal of Experimental Medicine,
vol. 2015, no. 7. Rockefeller University Press, pp. 1869–1890, 2018.
ista: Moalli F, Ficht X, Germann P, Vladymyrov M, Stolp B, de Vries I, Lyck R, Balmer
J, Fiocchi A, Kreutzfeldt M, Merkler D, Iannacone M, Ariga A, Stoffel MH, Sharpe
J, Bähler M, Sixt MK, Diz-Muñoz A, Stein JV. 2018. The Rho regulator Myosin IXb
enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental
Medicine. 2015(7), 1869–1890.
mla: Moalli, Federica, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid
Tissue Seeding of Protective CD8+T Cells.” The Journal of Experimental Medicine,
vol. 2015, no. 7, Rockefeller University Press, 2018, pp. 1869–1890, doi:10.1084/jem.20170896.
short: F. Moalli, X. Ficht, P. Germann, M. Vladymyrov, B. Stolp, I. de Vries, R.
Lyck, J. Balmer, A. Fiocchi, M. Kreutzfeldt, D. Merkler, M. Iannacone, A. Ariga,
M.H. Stoffel, J. Sharpe, M. Bähler, M.K. Sixt, A. Diz-Muñoz, J.V. Stein, The Journal
of Experimental Medicine 2015 (2018) 1869–1890.
date_created: 2019-05-28T12:36:47Z
date_published: 2018-06-06T00:00:00Z
date_updated: 2023-09-19T14:52:08Z
day: '06'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1084/jem.20170896
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- '000440822900011'
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issn:
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publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
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title: The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective
CD8+T cells
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legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
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volume: 2015
year: '2018'
...
---
_id: '437'
abstract:
- lang: eng
text: Dendritic cells (DCs) are sentinels of the adaptive immune system that reside
in peripheral organs of mammals. Upon pathogen encounter, they undergo maturation
and up-regulate the chemokine receptor CCR7 that guides them along gradients of
its chemokine ligands CCL19 and 21 to the next draining lymph node. There, DCs
present peripherally acquired antigen to naïve T cells, thereby triggering adaptive
immunity.
acknowledged_ssus:
- _id: SSU
acknowledgement: "This work was supported by grants of the European Research Council
(ERC CoG 724373) and the Austrian Science Fund (FWF) to M.S. We thank the scientific
support units at IST Austria for excellent technical support.\r\nWe thank the scientific
\ support units at IST Austria for excellent technical support. "
article_processing_charge: Yes (via OA deal)
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Hans
full_name: Haecker, Hans
last_name: Haecker
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Leithner AF, Renkawitz J, de Vries I, Hauschild R, Haecker H, Sixt MK. Fast
and efficient genetic engineering of hematopoietic precursor cells for the study
of dendritic cell migration. European Journal of Immunology. 2018;48(6):1074-1077.
doi:10.1002/eji.201747358
apa: Leithner, A. F., Renkawitz, J., de Vries, I., Hauschild, R., Haecker, H., &
Sixt, M. K. (2018). Fast and efficient genetic engineering of hematopoietic precursor
cells for the study of dendritic cell migration. European Journal of Immunology.
Wiley-Blackwell. https://doi.org/10.1002/eji.201747358
chicago: Leithner, Alexander F, Jörg Renkawitz, Ingrid de Vries, Robert Hauschild,
Hans Haecker, and Michael K Sixt. “Fast and Efficient Genetic Engineering of Hematopoietic
Precursor Cells for the Study of Dendritic Cell Migration.” European Journal
of Immunology. Wiley-Blackwell, 2018. https://doi.org/10.1002/eji.201747358.
ieee: A. F. Leithner, J. Renkawitz, I. de Vries, R. Hauschild, H. Haecker, and M.
K. Sixt, “Fast and efficient genetic engineering of hematopoietic precursor cells
for the study of dendritic cell migration,” European Journal of Immunology,
vol. 48, no. 6. Wiley-Blackwell, pp. 1074–1077, 2018.
ista: Leithner AF, Renkawitz J, de Vries I, Hauschild R, Haecker H, Sixt MK. 2018.
Fast and efficient genetic engineering of hematopoietic precursor cells for the
study of dendritic cell migration. European Journal of Immunology. 48(6), 1074–1077.
mla: Leithner, Alexander F., et al. “Fast and Efficient Genetic Engineering of Hematopoietic
Precursor Cells for the Study of Dendritic Cell Migration.” European Journal
of Immunology, vol. 48, no. 6, Wiley-Blackwell, 2018, pp. 1074–77, doi:10.1002/eji.201747358.
short: A.F. Leithner, J. Renkawitz, I. de Vries, R. Hauschild, H. Haecker, M.K.
Sixt, European Journal of Immunology 48 (2018) 1074–1077.
corr_author: '1'
date_created: 2018-12-11T11:46:28Z
date_published: 2018-02-13T00:00:00Z
date_updated: 2025-04-14T07:42:07Z
day: '13'
ddc:
- '570'
department:
- _id: MiSi
- _id: Bio
doi: 10.1002/eji.201747358
ec_funded: 1
external_id:
isi:
- '000434963700016'
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language:
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license: https://creativecommons.org/licenses/by-nc/4.0/
month: '02'
oa: 1
oa_version: Published Version
page: 1074 - 1077
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular Navigation Along Spatial Gradients
publication: European Journal of Immunology
publication_status: published
publisher: Wiley-Blackwell
publist_id: '7386'
pubrep_id: '1067'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Fast and efficient genetic engineering of hematopoietic precursor cells for
the study of dendritic cell migration
tmp:
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legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 48
year: '2018'
...
---
_id: '5672'
abstract:
- lang: eng
text: The release of IgM is the first line of an antibody response and precedes
the generation of high affinity IgG in germinal centers. Once secreted by freshly
activated plasmablasts, IgM is released into the efferent lymph of reactive lymph
nodes as early as 3 d after immunization. As pentameric IgM has an enormous size
of 1,000 kD, its diffusibility is low, and one might wonder how it can pass through
the densely lymphocyte-packed environment of a lymph node parenchyma in order
to reach its exit. In this issue of JEM, Thierry et al. show that, in order to
reach the blood stream, IgM molecules take a specific micro-anatomical route via
lymph node conduits.
article_processing_charge: No
author:
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- 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: Reversat A, Sixt MK. IgM’s exit route. Journal of Experimental Medicine.
2018;215(12):2959-2961. doi:10.1084/jem.20181934
apa: Reversat, A., & Sixt, M. K. (2018). IgM’s exit route. Journal of Experimental
Medicine. Rockefeller University Press. https://doi.org/10.1084/jem.20181934
chicago: Reversat, Anne, and Michael K Sixt. “IgM’s Exit Route.” Journal of Experimental
Medicine. Rockefeller University Press, 2018. https://doi.org/10.1084/jem.20181934.
ieee: A. Reversat and M. K. Sixt, “IgM’s exit route,” Journal of Experimental
Medicine, vol. 215, no. 12. Rockefeller University Press, pp. 2959–2961, 2018.
ista: Reversat A, Sixt MK. 2018. IgM’s exit route. Journal of Experimental Medicine.
215(12), 2959–2961.
mla: Reversat, Anne, and Michael K. Sixt. “IgM’s Exit Route.” Journal of Experimental
Medicine, vol. 215, no. 12, Rockefeller University Press, 2018, pp. 2959–61,
doi:10.1084/jem.20181934.
short: A. Reversat, M.K. Sixt, Journal of Experimental Medicine 215 (2018) 2959–2961.
date_created: 2018-12-16T22:59:18Z
date_published: 2018-11-20T00:00:00Z
date_updated: 2026-04-16T09:54:07Z
day: '20'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1084/jem.20181934
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- '000451920600002'
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oa: 1
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page: 2959-2961
publication: Journal of Experimental Medicine
publication_identifier:
issn:
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publication_status: published
publisher: Rockefeller University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: IgM's exit route
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
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short: CC BY-NC-SA (4.0)
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 215
year: '2018'
...
---
_id: '323'
abstract:
- lang: eng
text: 'In the here presented thesis, we explore the role of branched actin networks
in cell migration and antigen presentation, the two most relevant processes in
dendritic cell biology. Branched actin networks construct lamellipodial protrusions
at the leading edge of migrating cells. These are typically seen as adhesive structures,
which mediate force transduction to the extracellular matrix that leads to forward
locomotion. We ablated Arp2/3 nucleation promoting factor WAVE in DCs and found
that the resulting cells lack lamellipodial protrusions. Instead, depending on
the maturation state, one or multiple filopodia were formed. By challenging these
cells in a variety of migration assays we found that lamellipodial protrusions
are dispensable for the locomotion of leukocytes and actually dampen the speed
of migration. However, lamellipodia are critically required to negotiate complex
environments that DCs experience while they travel to the next draining lymph
node. Taken together our results suggest that leukocyte lamellipodia have rather
a sensory- than a force transducing function. Furthermore, we show for the first
time structure and dynamics of dendritic cell F-actin at the immunological synapse
with naïve T cells. Dendritic cell F-actin appears as dynamic foci that are nucleated
by the Arp2/3 complex. WAVE ablated dendritic cells show increased membrane tension,
leading to an altered ultrastructure of the immunological synapse and severe T
cell priming defects. These results point towards a previously unappreciated role
of the cellular mechanics of dendritic cells in T cell activation. Additionally,
we present a novel cell culture based system for the differentiation of dendritic
cells from conditionally immortalized hematopoietic precursors. These precursor
cells are genetically tractable via the CRISPR/Cas9 system while they retain their
ability to differentiate into highly migratory dendritic cells and other immune
cells. This will foster the study of all aspects of dendritic cell biology and
beyond. '
acknowledged_ssus:
- _id: NanoFab
- _id: Bio
- _id: PreCl
- _id: EM-Fac
acknowledgement: "First of all I would like to thank Michael Sixt for giving me the
opportunity to work in \r\nhis group and for his support throughout the years. He
is a truly inspiring person and \r\nthe best boss one can imagine. I would
\ also like to thank all current and past \r\nmembers of the Sixt group for
their help and the great working atmosphere in the lab. \r\nIt is a true privilege
to work with such a bright, funny and friendly group of people and \r\nI’m proud
\ that I could be part of it. Furthermore, I would like to say ‘thank
\ you’ to Daria Siekhaus for all the meetings and discussion we had throughout
the years \r\nand to Federica Benvenuti for being part of my committee.
\ I am also grateful to Jack \r\nMerrin in the nanofabrication facility
\ and all the people working in the bioimaging-\r\n, the electron microscopy-
and the preclinical facilities."
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
citation:
ama: Leithner AF. Branched actin networks in dendritic cell biology. 2018. doi:10.15479/AT:ISTA:th_998
apa: Leithner, A. F. (2018). Branched actin networks in dendritic cell biology.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_998
chicago: Leithner, Alexander F. “Branched Actin Networks in Dendritic Cell Biology.”
Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_998.
ieee: A. F. Leithner, “Branched actin networks in dendritic cell biology,” Institute
of Science and Technology Austria, 2018.
ista: Leithner AF. 2018. Branched actin networks in dendritic cell biology. Institute
of Science and Technology Austria.
mla: Leithner, Alexander F. Branched Actin Networks in Dendritic Cell Biology.
Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_998.
short: A.F. Leithner, Branched Actin Networks in Dendritic Cell Biology, Institute
of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2018-12-11T11:45:49Z
date_published: 2018-04-12T00:00:00Z
date_updated: 2025-09-22T08:27:34Z
day: '12'
ddc:
- '571'
- '599'
- '610'
degree_awarded: PhD
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:th_998
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language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: '99'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '7542'
pubrep_id: '998'
related_material:
record:
- id: '1321'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: Branched actin networks in dendritic cell biology
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2018'
...
---
_id: '15'
abstract:
- lang: eng
text: Although much is known about the physiological framework of T cell motility,
and numerous rate-limiting molecules have been identified through loss-of-function
approaches, an integrated functional concept of T cell motility is lacking. Here,
we used in vivo precision morphometry together with analysis of cytoskeletal dynamics
in vitro to deconstruct the basic mechanisms of T cell migration within lymphatic
organs. We show that the contributions of the integrin LFA-1 and the chemokine
receptor CCR7 are complementary rather than positioned in a linear pathway, as
they are during leukocyte extravasation from the blood vasculature. Our data demonstrate
that CCR7 controls cortical actin flows, whereas integrins mediate substrate friction
that is sufficient to drive locomotion in the absence of considerable surface
adhesions and plasma membrane flux.
acknowledged_ssus:
- _id: SSU
acknowledgement: This work was funded by grants from the European Research Council
(ERC StG 281556 and CoG 724373) and the Austrian Science Foundation (FWF) to M.S.
and by Swiss National Foundation (SNF) project grants 31003A_135649, 31003A_153457
and CR23I3_156234 to J.V.S. F.G. received funding from the European Union’s Horizon
2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement
no. 747687, and J.R. was funded by an EMBO long-term fellowship (ALTF 1396-2014).
article_processing_charge: No
author:
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Aglaja
full_name: Kopf, Aglaja
id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
last_name: Kopf
orcid: 0000-0002-2187-6656
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- 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: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Jörg
full_name: Renkawitz, Jörg
id: 3F0587C8-F248-11E8-B48F-1D18A9856A87
last_name: Renkawitz
orcid: 0000-0003-2856-3369
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- 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: Hons M, Kopf A, Hauschild R, et al. Chemokines and integrins independently
tune actin flow and substrate friction during intranodal migration of T cells.
Nature Immunology. 2018;19(6):606-616. doi:10.1038/s41590-018-0109-z
apa: Hons, M., Kopf, A., Hauschild, R., Leithner, A. F., Gärtner, F. R., Abe, J.,
… Sixt, M. K. (2018). Chemokines and integrins independently tune actin flow and
substrate friction during intranodal migration of T cells. Nature Immunology.
Nature Publishing Group. https://doi.org/10.1038/s41590-018-0109-z
chicago: Hons, Miroslav, Aglaja Kopf, Robert Hauschild, Alexander F Leithner, Florian
R Gärtner, Jun Abe, Jörg Renkawitz, Jens Stein, and Michael K Sixt. “Chemokines
and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal
Migration of T Cells.” Nature Immunology. Nature Publishing Group, 2018.
https://doi.org/10.1038/s41590-018-0109-z.
ieee: M. Hons et al., “Chemokines and integrins independently tune actin
flow and substrate friction during intranodal migration of T cells,” Nature
Immunology, vol. 19, no. 6. Nature Publishing Group, pp. 606–616, 2018.
ista: Hons M, Kopf A, Hauschild R, Leithner AF, Gärtner FR, Abe J, Renkawitz J,
Stein J, Sixt MK. 2018. Chemokines and integrins independently tune actin flow
and substrate friction during intranodal migration of T cells. Nature Immunology.
19(6), 606–616.
mla: Hons, Miroslav, et al. “Chemokines and Integrins Independently Tune Actin Flow
and Substrate Friction during Intranodal Migration of T Cells.” Nature Immunology,
vol. 19, no. 6, Nature Publishing Group, 2018, pp. 606–16, doi:10.1038/s41590-018-0109-z.
short: M. Hons, A. Kopf, R. Hauschild, A.F. Leithner, F.R. Gärtner, J. Abe, J. Renkawitz,
J. Stein, M.K. Sixt, Nature Immunology 19 (2018) 606–616.
date_created: 2018-12-11T11:44:10Z
date_published: 2018-05-18T00:00:00Z
date_updated: 2026-06-05T22:32:58Z
day: '18'
department:
- _id: MiSi
- _id: Bio
doi: 10.1038/s41590-018-0109-z
ec_funded: 1
external_id:
isi:
- '000433041500026'
pmid:
- '29777221'
intvolume: ' 19'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/29777221
month: '05'
oa: 1
oa_version: Published Version
page: 606 - 616
pmid: 1
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular Navigation Along Spatial Gradients
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
- _id: 25A48D24-B435-11E9-9278-68D0E5697425
grant_number: ALTF 1396-2014
name: Molecular and system level view of immune cell migration
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
publication: Nature Immunology
publication_status: published
publisher: Nature Publishing Group
publist_id: '8040'
quality_controlled: '1'
related_material:
record:
- id: '6891'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Chemokines and integrins independently tune actin flow and substrate friction
during intranodal migration of T cells
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 19
year: '2018'
...
---
_id: '402'
abstract:
- lang: eng
text: During metastasis, malignant cells escape the primary tumor, intravasate lymphatic
vessels, and reach draining sentinel lymph nodes before they colonize distant
organs via the blood circulation. Although lymph node metastasis in cancer patients
correlates with poor prognosis, evidence is lacking as to whether and how tumor
cells enter the bloodstream via lymph nodes. To investigate this question, we
delivered carcinoma cells into the lymph nodes of mice by microinfusing the cells
into afferent lymphatic vessels. We found that tumor cells rapidly infiltrated
the lymph node parenchyma, invaded blood vessels, and seeded lung metastases without
involvement of the thoracic duct. These results suggest that the lymph node blood
vessels can serve as an exit route for systemic dissemination of cancer cells
in experimental mouse models. Whether this form of tumor cell spreading occurs
in cancer patients remains to be determined.
acknowledged_ssus:
- _id: Bio
acknowledgement: "M.B. was supported by the Cell Communication in Health and Disease
graduate study program of the Austrian Science Fund (FWF) and the Medical University
of Vienna. M.S. was supported by the European Research Council (grant ERC GA 281556)
and an FWF START award.\r\nWe thank C. Moussion for establishing the intralymphatic
injection at IST Austria and for providing anti-PNAd hybridoma supernatant, R. Förster
and A. Braun for sharing the intralymphatic injection technology, K. Vaahtomeri
for the lentiviral constructs, M. Hons for establishing in vivo multiphoton imaging,
the Sixt lab for intellectual input, M. Schunn for help with the design of the in
vivo experiments, F. Langer for technical assistance with the in vivo experiments,
the bioimaging facility of IST Austria for support, and R. Efferl for providing
the CT26 cell line."
article_processing_charge: No
article_type: original
author:
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Helga
full_name: Schachner, Helga
last_name: Schachner
- first_name: Gabriele
full_name: Asfour, Gabriele
last_name: Asfour
- first_name: Zsuzsanna
full_name: Bagó Horváth, Zsuzsanna
last_name: Bagó Horváth
- first_name: Jens
full_name: Stein, Jens
last_name: Stein
- first_name: Pavel
full_name: Uhrin, Pavel
last_name: Uhrin
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
citation:
ama: Brown M, Assen FP, Leithner AF, et al. Lymph node blood vessels provide exit
routes for metastatic tumor cell dissemination in mice. Science. 2018;359(6382):1408-1411.
doi:10.1126/science.aal3662
apa: Brown, M., Assen, F. P., Leithner, A. F., Abe, J., Schachner, H., Asfour, G.,
… Kerjaschki, D. (2018). Lymph node blood vessels provide exit routes for metastatic
tumor cell dissemination in mice. Science. American Association for the
Advancement of Science. https://doi.org/10.1126/science.aal3662
chicago: Brown, Markus, Frank P Assen, Alexander F Leithner, Jun Abe, Helga Schachner,
Gabriele Asfour, Zsuzsanna Bagó Horváth, et al. “Lymph Node Blood Vessels Provide
Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” Science.
American Association for the Advancement of Science, 2018. https://doi.org/10.1126/science.aal3662.
ieee: M. Brown et al., “Lymph node blood vessels provide exit routes for
metastatic tumor cell dissemination in mice,” Science, vol. 359, no. 6382.
American Association for the Advancement of Science, pp. 1408–1411, 2018.
ista: Brown M, Assen FP, Leithner AF, Abe J, Schachner H, Asfour G, Bagó Horváth
Z, Stein J, Uhrin P, Sixt MK, Kerjaschki D. 2018. Lymph node blood vessels provide
exit routes for metastatic tumor cell dissemination in mice. Science. 359(6382),
1408–1411.
mla: Brown, Markus, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic
Tumor Cell Dissemination in Mice.” Science, vol. 359, no. 6382, American
Association for the Advancement of Science, 2018, pp. 1408–11, doi:10.1126/science.aal3662.
short: M. Brown, F.P. Assen, A.F. Leithner, J. Abe, H. Schachner, G. Asfour, Z.
Bagó Horváth, J. Stein, P. Uhrin, M.K. Sixt, D. Kerjaschki, Science 359 (2018)
1408–1411.
corr_author: '1'
date_created: 2018-12-11T11:46:16Z
date_published: 2018-03-23T00:00:00Z
date_updated: 2026-06-05T22:34:18Z
day: '23'
department:
- _id: MiSi
doi: 10.1126/science.aal3662
ec_funded: 1
external_id:
isi:
- '000428043600047'
pmid:
- '29567714'
intvolume: ' 359'
isi: 1
issue: '6382'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1126/science.aal3662
month: '03'
oa: 1
oa_version: Published Version
page: 1408 - 1411
pmid: 1
project:
- _id: 25A8E5EA-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Y 564-B12
name: Cytoskeletal force generation and force transduction of migrating leukocytes
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7428'
quality_controlled: '1'
related_material:
record:
- id: '6947'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination
in mice
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 359
year: '2018'
...
---
OA_place: publisher
OA_type: free access
_id: '1161'
abstract:
- lang: eng
text: Coordinated changes of cell shape are often the result of the excitable, wave-like
dynamics of the actin cytoskeleton. New work shows that, in migrating cells, protrusion
waves arise from mechanochemical crosstalk between adhesion sites, membrane tension
and the actin protrusive machinery.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: 'Müller J, Sixt MK. Cell migration: Making the waves. Current Biology.
2017;27(1):R24-R25. doi:10.1016/j.cub.2016.11.035'
apa: 'Müller, J., & Sixt, M. K. (2017). Cell migration: Making the waves. Current
Biology. Cell Press. https://doi.org/10.1016/j.cub.2016.11.035'
chicago: 'Müller, Jan, and Michael K Sixt. “Cell Migration: Making the Waves.” Current
Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2016.11.035.'
ieee: 'J. Müller and M. K. Sixt, “Cell migration: Making the waves,” Current
Biology, vol. 27, no. 1. Cell Press, pp. R24–R25, 2017.'
ista: 'Müller J, Sixt MK. 2017. Cell migration: Making the waves. Current Biology.
27(1), R24–R25.'
mla: 'Müller, Jan, and Michael K. Sixt. “Cell Migration: Making the Waves.” Current
Biology, vol. 27, no. 1, Cell Press, 2017, pp. R24–25, doi:10.1016/j.cub.2016.11.035.'
short: J. Müller, M.K. Sixt, Current Biology 27 (2017) R24–R25.
date_created: 2018-12-11T11:50:29Z
date_published: 2017-01-09T00:00:00Z
date_updated: 2025-06-26T09:01:10Z
day: '09'
department:
- _id: MiSi
doi: 10.1016/j.cub.2016.11.035
external_id:
isi:
- '000391902500010'
intvolume: ' 27'
isi: 1
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cub.2016.11.035
month: '01'
oa: 1
oa_version: Published Version
page: R24 - R25
publication: Current Biology
publication_identifier:
issn:
- '09609822'
publication_status: published
publisher: Cell Press
publist_id: '6197'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Cell migration: Making the waves'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 27
year: '2017'
...