---
OA_type: free access
_id: '3167'
article_processing_charge: No
article_type: letter_note
author:
- first_name: Michele
full_name: Weber, Michele
id: 3A3FC708-F248-11E8-B48F-1D18A9856A87
last_name: Weber
citation:
ama: Weber M. NextGen speaks 13 . Science. 2012;336(6077):32-34. doi:10.1126/science.336.6077.32
apa: Weber, M. (2012). NextGen speaks 13 . Science. American Association
for the Advancement of Science. https://doi.org/10.1126/science.336.6077.32
chicago: Weber, Michele. “NextGen Speaks 13 .” Science. American Association
for the Advancement of Science, 2012. https://doi.org/10.1126/science.336.6077.32.
ieee: M. Weber, “NextGen speaks 13 ,” Science, vol. 336, no. 6077. American
Association for the Advancement of Science, pp. 32–34, 2012.
ista: Weber M. 2012. NextGen speaks 13 . Science. 336(6077), 32–34.
mla: Weber, Michele. “NextGen Speaks 13 .” Science, vol. 336, no. 6077, American
Association for the Advancement of Science, 2012, pp. 32–34, doi:10.1126/science.336.6077.32.
short: M. Weber, Science 336 (2012) 32–34.
date_created: 2018-12-11T12:01:47Z
date_published: 2012-04-06T00:00:00Z
date_updated: 2025-05-20T07:14:51Z
day: '06'
department:
- _id: MiSi
doi: 10.1126/science.336.6077.32
external_id:
pmid:
- '22491839'
fulldoi: https://doi.org/10.1126/science.336.6077.32
intvolume: ' 336'
issue: '6077'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1126/science.336.6077.32
month: '04'
oa: 1
oa_version: None
page: 32-34
pmid: 1
popular_science: '1'
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '3516'
status: public
title: 'NextGen speaks 13 '
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 336
year: '2012'
...
---
_id: '506'
article_processing_charge: No
article_type: original
author:
- 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: 'Sixt MK. Cell migration: Fibroblasts find a new way to get ahead. Journal
of Cell Biology. 2012;197(3):347-349. doi:10.1083/jcb.201204039'
apa: 'Sixt, M. K. (2012). Cell migration: Fibroblasts find a new way to get ahead.
Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201204039'
chicago: 'Sixt, Michael K. “Cell Migration: Fibroblasts Find a New Way to Get Ahead.”
Journal of Cell Biology. Rockefeller University Press, 2012. https://doi.org/10.1083/jcb.201204039.'
ieee: 'M. K. Sixt, “Cell migration: Fibroblasts find a new way to get ahead,” Journal
of Cell Biology, vol. 197, no. 3. Rockefeller University Press, pp. 347–349,
2012.'
ista: 'Sixt MK. 2012. Cell migration: Fibroblasts find a new way to get ahead. Journal
of Cell Biology. 197(3), 347–349.'
mla: 'Sixt, Michael K. “Cell Migration: Fibroblasts Find a New Way to Get Ahead.”
Journal of Cell Biology, vol. 197, no. 3, Rockefeller University Press,
2012, pp. 347–49, doi:10.1083/jcb.201204039.'
short: M.K. Sixt, Journal of Cell Biology 197 (2012) 347–349.
corr_author: '1'
das_tickbox: '1'
date_created: 2018-12-11T11:46:51Z
date_published: 2012-04-30T00:00:00Z
date_updated: 2026-07-28T09:22:21Z
day: '30'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1083/jcb.201204039
external_id:
isi:
- '000303467800004'
file:
- access_level: open_access
checksum: 45c02be33ebd99fc3077d60b9c90bdfa
content_type: application/pdf
creator: kschuh
date_created: 2019-02-12T09:03:09Z
date_updated: 2020-07-14T12:46:36Z
file_id: '5957'
file_name: 2012_CellBiology_Sixt.pdf
file_size: 986566
relation: main_file
file_date_updated: 2020-07-14T12:46:36Z
fulldoi: https://doi.org/10.1083/jcb.201204039
has_accepted_license: '1'
intvolume: ' 197'
isi: 1
issue: '3'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-sa/3.0/
month: '04'
oa: 1
oa_version: Published Version
page: 347 - 349
publication: Journal of Cell Biology
publication_status: published
publisher: Rockefeller University Press
publist_id: '7314'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Cell migration: Fibroblasts find a new way to get ahead'
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/3.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported (CC BY-NC-SA
3.0)
short: CC BY-NC-SA (3.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 197
year: '2012'
...
---
_id: '491'
abstract:
- lang: eng
text: In their search for antigens, lymphocytes continuously shuttle among blood
vessels, lymph vessels, and lymphatic tissues. Chemokines mediate entry of lymphocytes
into lymphatic tissues, and sphingosine 1-phosphate (S1P) promotes localization
of lymphocytes to the vasculature. Both signals are sensed through G protein-coupled
receptors (GPCRs). Most GPCRs undergo ligand-dependent homologous receptor desensitization,
a process that decreases their signaling output after previous exposure to high
ligand concentration. Such desensitization can explain why lymphocytes do not
take an intermediate position between two signals but rather oscillate between
them. The desensitization of S1P receptor 1 (S1PR1) is mediated by GPCR kinase
2 (GRK2). Deletion of GRK2 in lymphocytes compromises desensitization by high
vascular S1P concentrations, thereby reducing responsiveness to the chemokine
signal and trapping the cells in the vascular compartment. The desensitization
kinetics of S1PR1 allows lymphocytes to dynamically shuttle between vasculature
and lymphatic tissue, although the positional information in both compartments
is static.
article_number: pe43
article_processing_charge: No
author:
- first_name: Alexander
full_name: Eichner, Alexander
id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87
last_name: Eichner
- 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: Eichner A, Sixt MK. Setting the clock for recirculating lymphocytes. Science
Signaling. 2011;4(198). doi:10.1126/scisignal.2002617
apa: Eichner, A., & Sixt, M. K. (2011). Setting the clock for recirculating
lymphocytes. Science Signaling. American Association for the Advancement
of Science. https://doi.org/10.1126/scisignal.2002617
chicago: Eichner, Alexander, and Michael K Sixt. “Setting the Clock for Recirculating
Lymphocytes.” Science Signaling. American Association for the Advancement
of Science, 2011. https://doi.org/10.1126/scisignal.2002617.
ieee: A. Eichner and M. K. Sixt, “Setting the clock for recirculating lymphocytes,”
Science Signaling, vol. 4, no. 198. American Association for the Advancement
of Science, 2011.
ista: Eichner A, Sixt MK. 2011. Setting the clock for recirculating lymphocytes.
Science Signaling. 4(198), pe43.
mla: Eichner, Alexander, and Michael K. Sixt. “Setting the Clock for Recirculating
Lymphocytes.” Science Signaling, vol. 4, no. 198, pe43, American Association
for the Advancement of Science, 2011, doi:10.1126/scisignal.2002617.
short: A. Eichner, M.K. Sixt, Science Signaling 4 (2011).
corr_author: '1'
date_created: 2018-12-11T11:46:46Z
date_published: 2011-11-08T00:00:00Z
date_updated: 2025-09-30T09:24:17Z
day: '08'
department:
- _id: MiSi
doi: 10.1126/scisignal.2002617
external_id:
isi:
- '000296800500002'
fulldoi: https://doi.org/10.1126/scisignal.2002617
intvolume: ' 4'
isi: 1
issue: '198'
language:
- iso: eng
month: '11'
oa_version: None
publication: Science Signaling
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7329'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Setting the clock for recirculating lymphocytes
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 4
year: '2011'
...
---
_id: '518'
abstract:
- lang: eng
text: Cancer stem cells or cancer initiating cells are believed to contribute to
cancer recurrence after therapy. MicroRNAs (miRNAs) are short RNA molecules with
fundamental roles in gene regulation. The role of miRNAs in cancer stem cells
is only poorly understood. Here, we report miRNA expression profiles of glioblastoma
stem cell-containing CD133 + cell populations. We find that miR-9, miR-9 * (referred
to as miR-9/9 *), miR-17 and miR-106b are highly abundant in CD133 + cells. Furthermore,
inhibition of miR-9/9 * or miR-17 leads to reduced neurosphere formation and stimulates
cell differentiation. Calmodulin-binding transcription activator 1 (CAMTA1) is
a putative transcription factor, which induces the expression of the anti-proliferative
cardiac hormone natriuretic peptide A (NPPA). We identify CAMTA1 as an miR-9/9
* and miR-17 target. CAMTA1 expression leads to reduced neurosphere formation
and tumour growth in nude mice, suggesting that CAMTA1 can function as tumour
suppressor. Consistently, CAMTA1 and NPPA expression correlate with patient survival.
Our findings could provide a basis for novel strategies of glioblastoma therapy.
article_processing_charge: No
article_type: original
author:
- first_name: Daniel
full_name: Schraivogel, Daniel
last_name: Schraivogel
- first_name: Lasse
full_name: Weinmann, Lasse
last_name: Weinmann
- first_name: Dagmar
full_name: Beier, Dagmar
last_name: Beier
- first_name: Ghazaleh
full_name: Tabatabai, Ghazaleh
last_name: Tabatabai
- first_name: Alexander
full_name: Eichner, Alexander
id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87
last_name: Eichner
- first_name: Jia
full_name: Zhu, Jia
last_name: Zhu
- first_name: Martina
full_name: Anton, Martina
last_name: Anton
- 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: Michael
full_name: Weller, Michael
last_name: Weller
- first_name: Christoph
full_name: Beier, Christoph
last_name: Beier
- first_name: Gunter
full_name: Meister, Gunter
last_name: Meister
citation:
ama: Schraivogel D, Weinmann L, Beier D, et al. CAMTA1 is a novel tumour suppressor
regulated by miR-9/9 * in glioblastoma stem cells. EMBO Journal. 2011;30(20):4309-4322.
doi:10.1038/emboj.2011.301
apa: Schraivogel, D., Weinmann, L., Beier, D., Tabatabai, G., Eichner, A., Zhu,
J., … Meister, G. (2011). CAMTA1 is a novel tumour suppressor regulated by miR-9/9
* in glioblastoma stem cells. EMBO Journal. Wiley-Blackwell. https://doi.org/10.1038/emboj.2011.301
chicago: Schraivogel, Daniel, Lasse Weinmann, Dagmar Beier, Ghazaleh Tabatabai,
Alexander Eichner, Jia Zhu, Martina Anton, et al. “CAMTA1 Is a Novel Tumour Suppressor
Regulated by MiR-9/9 * in Glioblastoma Stem Cells.” EMBO Journal. Wiley-Blackwell,
2011. https://doi.org/10.1038/emboj.2011.301.
ieee: D. Schraivogel et al., “CAMTA1 is a novel tumour suppressor regulated
by miR-9/9 * in glioblastoma stem cells,” EMBO Journal, vol. 30, no. 20.
Wiley-Blackwell, pp. 4309–4322, 2011.
ista: Schraivogel D, Weinmann L, Beier D, Tabatabai G, Eichner A, Zhu J, Anton M,
Sixt MK, Weller M, Beier C, Meister G. 2011. CAMTA1 is a novel tumour suppressor
regulated by miR-9/9 * in glioblastoma stem cells. EMBO Journal. 30(20), 4309–4322.
mla: Schraivogel, Daniel, et al. “CAMTA1 Is a Novel Tumour Suppressor Regulated
by MiR-9/9 * in Glioblastoma Stem Cells.” EMBO Journal, vol. 30, no. 20,
Wiley-Blackwell, 2011, pp. 4309–22, doi:10.1038/emboj.2011.301.
short: D. Schraivogel, L. Weinmann, D. Beier, G. Tabatabai, A. Eichner, J. Zhu,
M. Anton, M.K. Sixt, M. Weller, C. Beier, G. Meister, EMBO Journal 30 (2011) 4309–4322.
date_created: 2018-12-11T11:46:55Z
date_published: 2011-10-19T00:00:00Z
date_updated: 2025-09-30T09:23:51Z
day: '19'
department:
- _id: MiSi
doi: 10.1038/emboj.2011.301
external_id:
isi:
- '000296715800018'
pmid:
- '21857646'
fulldoi: https://doi.org/10.1038/emboj.2011.301
intvolume: ' 30'
isi: 1
issue: '20'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199389/
month: '10'
oa: 1
oa_version: Submitted Version
page: 4309 - 4322
pmid: 1
publication: EMBO Journal
publication_status: published
publisher: Wiley-Blackwell
publist_id: '7301'
quality_controlled: '1'
scopus_import: '1'
status: public
title: CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma
stem cells
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 30
year: '2011'
...
---
OA_place: publisher
_id: '3275'
abstract:
- lang: eng
text: 'Chemokines organize immune cell trafficking by inducing either directed (tactic)
or random (kinetic) migration and by activating integrins in order to support
surface adhesion (haptic). Beyond that the same chemokines can establish clearly
defined functional areas in secondary lymphoid organs. Until now it is unclear
how chemokines can fulfill such diverse functions. One decisive prerequisite to
explain these capacities is to know how chemokines are presented in tissue. In
theory chemokines could occur either soluble or immobilized, and could be distributed
either homogenously or as a concentration gradient. To dissect if and how the
presenting mode of chemokines influences immune cells, I tested the response of
dendritic cells (DCs) to differentially displayed chemokines. DCs are antigen
presenting cells that reside in the periphery and migrate into draining lymph
nodes (LNs) once exposed to inflammatory stimuli to activate naïve T cells. DCs
are guided to and within the LN by the chemokine receptor CCR7, which has two
ligands, the chemokines CCL19 and CCL21. Both CCR7 ligands are expressed by fibroblastic
reticular cells in the LN, but differ in their ability to bind to heparan sulfate
residues. CCL21 has a highly charged C-terminal extension, which mediates binding
to anionic surfaces, whereas CCL19 is lacking such residues and likely distributes
as a soluble molecule. This study shows that surface-bound CCL21 causes random,
haptokinetic DC motility, which is confined to the chemokine coated area by insideout
activation of β2 integrins that mediate cell binding to the surface. CCL19 on
the other hand forms concentration gradients which trigger directional, chemotactic
movement, but no surface adhesion. In addition DCs can actively manipulate this
system by recruiting and activating serine proteases on their surfaces, which
create - by proteolytically removing the adhesive C-terminus - a solubilized variant
of CCL21 that functionally resembles CCL19. By generating a CCL21 concentration
gradient DCs establish a positive feedback loop to recruit further DCs from the
periphery to the CCL21 coated region. In addition DCs can sense chemotactic gradients
as well as immobilized haptokinetic fields at the same time and integrate these
signals. The result is chemotactically biased haptokinesis - directional migration
confined to a chemokine coated track or area - which could explain the dynamic
but spatially tightly controlled swarming leukocyte locomotion patterns that have
been observed in lymphatic organs by intravital microscopists. The finding that
DCs can approach soluble cues in a non-adhesive manner while they attach to surfaces
coated with immobilized cues raises the question how these cells transmit intracellular
forces to the environment, especially in the non-adherent migration mode. In order
to migrate, cells have to generate and transmit force to the extracellular substrate.
Force transmission is the prerequisite to procure an expansion of the leading
edge and a forward motion of the whole cell body. In the current conceptions actin
polymerization at the leading edge is coupled to extracellular ligands via the
integrin family of transmembrane receptors, which allows the transmission of intracellular
force. Against the paradigm of force transmission during migration, leukocytes,
like DCs, are able to migrate in threedimensional environments without using integrin
transmembrane receptors (Lämmermann et al., 2008). This reflects the biological
function of leukocytes, as they can invade almost all tissues, whereby their migration
has to be independent from the extracellular environment. How the cells can achieve
this is unclear. For this study I examined DC migration in a defined threedimensional
environment and highlighted actin-dynamics with the probe Lifeact-GFP. The result
was that chemotactic DCs can switch between integrin-dependent and integrin- independent
locomotion and can thereby adapt to the adhesive properties of their environment.
If the cells are able to couple their actin cytoskeleton to the substrate, actin
polymerization is entirely converted into protrusion. Without coupling the actin
cortex undergoes slippage and retrograde actin flow can be observed. But retrograde
actin flow can be completely compensated by higher actin polymerization rate keeping
the migration velocity and the shape of the cells unaltered. Mesenchymal cells
like fibroblast cannot balance the loss of adhesive interaction, cannot protrude
into open space and, therefore, strictly depend on integrinmediated force coupling.
This leukocyte specific phenomenon of “adaptive force transmission” endows these
cells with the unique ability to transit and invade almost every type of tissue. '
acknowledgement: "I would like to express my sincere gratitude to the following people
who made with their continuous support and encouragement this thesis possible: First,
I want to thank Prof. Dr. Michael Sixt for his excellent supervision and mentoring,
especially for the nice, relaxed working atmosphere, a lot of brilliant ideas and
the freedom to work in my own way.\r\n\r\nProf. Dr. Reinhard Fässler for his constant
support of the Sixt lab and for providing excellent working conditions. \r\n\r\nProf.
Dr. Sanjiv Luther and Prof. Dr. Tobias Bollenbach for agreeing to be member of my
thesis committee and to evaluate my work.\r\n\r\nDr. Walther Göhring, Carmen Schmitz,
the Recombinant Protein Production core facility and the animal care takers for
providing the “infrastructure” for this thesis. \r\n\r\nProf. Dr. Daniel Legler,
Markus Bruckner and Dr. Julien Polleux for very fruitful collaborations and discussions.\r\n\r\nMy
labmates for their help, a lot of discussions and to make the Sixt lab to a convenient
place to work : Karin Hirsch, Tim Lämmeramnn, Holger Pflicke, Jörg Renkawitz, Michele
Weber and Alexander Eichner All members of the Department of Molecular Medicine
for their help. Especially I want to thank Sarah Schmidt, Karin Hirsch and Raphael
Ruppert for their friendship, nice chats and their uncensored point of view. "
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Kathrin
full_name: Schumann, Kathrin
id: F44D762E-4F9D-11E9-B64C-9EB26CEFFB5F
last_name: Schumann
citation:
ama: Schumann K. The role of chemotactic gradients in dendritic cell migration.
2011.
apa: Schumann, K. (2011). The role of chemotactic gradients in dendritic cell
migration. Institute of Science and Technology Austria.
chicago: Schumann, Kathrin. “The Role of Chemotactic Gradients in Dendritic Cell
Migration.” Institute of Science and Technology Austria, 2011.
ieee: K. Schumann, “The role of chemotactic gradients in dendritic cell migration,”
Institute of Science and Technology Austria, 2011.
ista: Schumann K. 2011. The role of chemotactic gradients in dendritic cell migration.
Institute of Science and Technology Austria.
mla: Schumann, Kathrin. The Role of Chemotactic Gradients in Dendritic Cell Migration.
Institute of Science and Technology Austria, 2011.
short: K. Schumann, The Role of Chemotactic Gradients in Dendritic Cell Migration,
Institute of Science and Technology Austria, 2011.
corr_author: '1'
date_created: 2018-12-11T12:02:24Z
date_published: 2011-03-01T00:00:00Z
date_updated: 2026-04-09T14:36:24Z
day: '01'
ddc:
- '570'
- '579'
degree_awarded: PhD
department:
- _id: MiSi
file:
- access_level: closed
checksum: e69eee6252660f0b694a2ea8923ddc72
content_type: application/pdf
creator: dernst
date_created: 2019-03-26T08:12:21Z
date_updated: 2020-07-14T12:46:06Z
file_id: '6177'
file_name: 2011_Thesis_Kathrin_Schumann.pdf
file_size: 4487708
relation: main_file
- access_level: open_access
checksum: 71727d63f424b5b446f68f4b87ecadc0
content_type: application/pdf
creator: dernst
date_created: 2021-02-22T11:24:30Z
date_updated: 2021-02-22T11:24:30Z
file_id: '9175'
file_name: 2011_Thesis_Schumann_noS.pdf
file_size: 4313127
relation: main_file
success: 1
file_date_updated: 2021-02-22T11:24:30Z
has_accepted_license: '1'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: '141'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '3371'
pubrep_id: '11'
status: public
supervisor:
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
title: The role of chemotactic gradients in dendritic cell migration
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2011'
...
---
_id: '3287'
abstract:
- lang: eng
text: 'Diffusing membrane constituents are constantly exposed to a variety of forces
that influence their stochastic path. Single molecule experiments allow for resolving
trajectories at extremely high spatial and temporal accuracy, thereby offering
insights into en route interactions of the tracer. In this review we discuss approaches
to derive information about the underlying processes, based on single molecule
tracking experiments. In particular, we focus on a new versatile way to analyze
single molecule diffusion in the absence of a full analytical treatment. The method
is based on comprehensive comparison of an experimental data set against the hypothetical
outcome of multiple experiments performed on the computer. Since Monte Carlo simulations
can be easily and rapidly performed even on state-of-the-art PCs, our method provides
a simple way for testing various - even complicated - diffusion models. We describe
the new method in detail, and show the applicability on two specific examples:
firstly, kinetic rate constants can be derived for the transient interaction of
mobile membrane proteins; secondly, residence time and corral size can be extracted
for confined diffusion.'
article_processing_charge: No
author:
- first_name: Verena
full_name: Ruprecht, Verena
id: 4D71A03A-F248-11E8-B48F-1D18A9856A87
last_name: Ruprecht
orcid: 0000-0003-4088-8633
- first_name: Markus
full_name: Axmann, Markus
last_name: Axmann
- first_name: Stefan
full_name: Wieser, Stefan
id: 355AA5A0-F248-11E8-B48F-1D18A9856A87
last_name: Wieser
orcid: 0000-0002-2670-2217
- first_name: Gerhard
full_name: Schuetz, Gerhard
last_name: Schuetz
citation:
ama: Ruprecht V, Axmann M, Wieser S, Schuetz G. What can we learn from single molecule
trajectories? Current Protein & Peptide Science. 2011;12(8):714-724.
doi:10.2174/138920311798841753
apa: Ruprecht, V., Axmann, M., Wieser, S., & Schuetz, G. (2011). What can we
learn from single molecule trajectories? Current Protein & Peptide Science.
Bentham Science Publishers. https://doi.org/10.2174/138920311798841753
chicago: Ruprecht, Verena, Markus Axmann, Stefan Wieser, and Gerhard Schuetz. “What
Can We Learn from Single Molecule Trajectories?” Current Protein & Peptide
Science. Bentham Science Publishers, 2011. https://doi.org/10.2174/138920311798841753.
ieee: V. Ruprecht, M. Axmann, S. Wieser, and G. Schuetz, “What can we learn from
single molecule trajectories?,” Current Protein & Peptide Science,
vol. 12, no. 8. Bentham Science Publishers, pp. 714–724, 2011.
ista: Ruprecht V, Axmann M, Wieser S, Schuetz G. 2011. What can we learn from single
molecule trajectories? Current Protein & Peptide Science. 12(8), 714–724.
mla: Ruprecht, Verena, et al. “What Can We Learn from Single Molecule Trajectories?”
Current Protein & Peptide Science, vol. 12, no. 8, Bentham Science
Publishers, 2011, pp. 714–24, doi:10.2174/138920311798841753.
short: V. Ruprecht, M. Axmann, S. Wieser, G. Schuetz, Current Protein & Peptide
Science 12 (2011) 714–724.
date_created: 2018-12-11T12:02:28Z
date_published: 2011-12-01T00:00:00Z
date_updated: 2025-09-30T09:21:31Z
day: '01'
department:
- _id: CaHe
- _id: MiSi
doi: 10.2174/138920311798841753
external_id:
isi:
- '000299672600005'
fulldoi: https://doi.org/10.2174/138920311798841753
intvolume: ' 12'
isi: 1
issue: '8'
language:
- iso: eng
month: '12'
oa_version: None
page: 714 - 724
publication: Current Protein & Peptide Science
publication_status: published
publisher: Bentham Science Publishers
publist_id: '3358'
quality_controlled: '1'
scopus_import: '1'
status: public
title: What can we learn from single molecule trajectories?
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 12
year: '2011'
...
---
_id: '3371'
abstract:
- lang: eng
text: The Minisymposium “Cell Migration and Motility” was attended by approximately
500 visitors and covered a broad range of questions in the field using diverse
model systems. Topics comprised actin dynamics, cell polarity, force transduction,
signal transduction, bar- rier transmigration, and chemotactic guidance.
article_processing_charge: No
article_type: original
author:
- 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: Carole
full_name: Parent, Carole
last_name: Parent
citation:
ama: Sixt MK, Parent C. Cells on the move in Philadelphia. Molecular Biology
and Evolution. 2011;22(6):724. doi:10.1091/mbc.E10-12-0958
apa: Sixt, M. K., & Parent, C. (2011). Cells on the move in Philadelphia. Molecular
Biology and Evolution. Oxford University Press. https://doi.org/10.1091/mbc.E10-12-0958
chicago: Sixt, Michael K, and Carole Parent. “Cells on the Move in Philadelphia.”
Molecular Biology and Evolution. Oxford University Press, 2011. https://doi.org/10.1091/mbc.E10-12-0958.
ieee: M. K. Sixt and C. Parent, “Cells on the move in Philadelphia,” Molecular
Biology and Evolution, vol. 22, no. 6. Oxford University Press, p. 724, 2011.
ista: Sixt MK, Parent C. 2011. Cells on the move in Philadelphia. Molecular Biology
and Evolution. 22(6), 724.
mla: Sixt, Michael K., and Carole Parent. “Cells on the Move in Philadelphia.” Molecular
Biology and Evolution, vol. 22, no. 6, Oxford University Press, 2011, p. 724,
doi:10.1091/mbc.E10-12-0958.
short: M.K. Sixt, C. Parent, Molecular Biology and Evolution 22 (2011) 724.
date_created: 2018-12-11T12:02:57Z
date_published: 2011-03-15T00:00:00Z
date_updated: 2025-09-30T08:58:51Z
day: '15'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1091/mbc.E10-12-0958
external_id:
isi:
- '000288368200010'
file:
- access_level: open_access
checksum: 3467986ab7a64e7694ffd1013b5d9da9
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:29Z
date_updated: 2020-07-14T12:46:11Z
file_id: '5283'
file_name: IST-2015-373-v1+1_Mol._Biol._Cell-2011-Sixt-724.pdf
file_size: 105421
relation: main_file
file_date_updated: 2020-07-14T12:46:11Z
fulldoi: https://doi.org/10.1091/mbc.E10-12-0958
has_accepted_license: '1'
intvolume: ' 22'
isi: 1
issue: '6'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-sa/4.0/
month: '03'
oa: 1
oa_version: Published Version
page: '724'
publication: Molecular Biology and Evolution
publication_status: published
publisher: Oxford University Press
publist_id: '3238'
pubrep_id: '373'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Cells on the move in Philadelphia
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 22
year: '2011'
...
---
_id: '3385'
article_processing_charge: No
article_type: review
author:
- 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: Sixt MK. Interstitial locomotion of leukocytes. Immunology Letters.
2011;138(1):32-34. doi:10.1016/j.imlet.2011.02.013
apa: Sixt, M. K. (2011). Interstitial locomotion of leukocytes. Immunology Letters.
Elsevier. https://doi.org/10.1016/j.imlet.2011.02.013
chicago: Sixt, Michael K. “Interstitial Locomotion of Leukocytes.” Immunology
Letters. Elsevier, 2011. https://doi.org/10.1016/j.imlet.2011.02.013.
ieee: M. K. Sixt, “Interstitial locomotion of leukocytes,” Immunology Letters,
vol. 138, no. 1. Elsevier, pp. 32–34, 2011.
ista: Sixt MK. 2011. Interstitial locomotion of leukocytes. Immunology Letters.
138(1), 32–34.
mla: Sixt, Michael K. “Interstitial Locomotion of Leukocytes.” Immunology Letters,
vol. 138, no. 1, Elsevier, 2011, pp. 32–34, doi:10.1016/j.imlet.2011.02.013.
short: M.K. Sixt, Immunology Letters 138 (2011) 32–34.
corr_author: '1'
date_created: 2018-12-11T12:03:02Z
date_published: 2011-07-01T00:00:00Z
date_updated: 2025-09-30T08:47:13Z
day: '01'
department:
- _id: MiSi
doi: 10.1016/j.imlet.2011.02.013
external_id:
isi:
- '000292714800011'
fulldoi: https://doi.org/10.1016/j.imlet.2011.02.013
intvolume: ' 138'
isi: 1
issue: '1'
language:
- iso: eng
month: '07'
oa_version: None
page: 32 - 34
publication: Immunology Letters
publication_status: published
publisher: Elsevier
publist_id: '3222'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Interstitial locomotion of leukocytes
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 138
year: '2011'
...
---
_id: '3392'
abstract:
- lang: eng
text: Migrating lymphocytes acquire a polarized phenotype with a leading and a trailing
edge, or uropod. Although in vitro experiments in cell lines or activated primary
cell cultures have established that Rho-p160 coiled-coil kinase (ROCK)-myosin
II-mediated uropod contractility is required for integrin de-adhesion on two-dimensional
surfaces and nuclear propulsion through narrow pores in three-dimensional matrices,
less is known about the role of these two events during the recirculation of primary,
nonactivated lymphocytes. Using pharmacological antagonists of ROCK and myosin
II, we report that inhibition of uropod contractility blocked integrin-independent
mouse T cell migration through narrow, but not large, pores in vitro. T cell crawling
on chemokine-coated endothelial cells under shear was severely impaired by ROCK
inhibition, whereas transendothelial migration was only reduced through endothelial
cells with high, but not low, barrier properties. Using three-dimensional thick-tissue
imaging and dynamic two-photon microscopy of T cell motility in lymphoid tissue,
we demonstrated a significant role for uropod contractility in intraluminal crawling
and transendothelial migration through lymph node, but not bone marrow, endothelial
cells. Finally, we demonstrated that ICAM-1, but not anatomical constraints or
integrin-independent interactions, reduced parenchymal motility of inhibitor-treated
T cells within the dense lymphoid microenvironment, thus assigning context-dependent
roles for uropod contraction during lymphocyte recirculation.
article_processing_charge: No
article_type: original
author:
- first_name: Silvia
full_name: Soriano, Silvia
last_name: Soriano
- first_name: Miroslav
full_name: Hons, Miroslav
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Kathrin
full_name: Schumann, Kathrin
last_name: Schumann
- first_name: Varsha
full_name: Kumar, Varsha
last_name: Kumar
- first_name: Timo
full_name: Dennier, Timo
last_name: Dennier
- first_name: Ruth
full_name: Lyck, Ruth
last_name: Lyck
- 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: Jens
full_name: Stein, Jens
last_name: Stein
citation:
ama: Soriano S, Hons M, Schumann K, et al. In vivo analysis of uropod function during
physiological T cell trafficking. Journal of Immunology. 2011;187(5):2356-2364.
doi:10.4049/jimmunol.1100935
apa: Soriano, S., Hons, M., Schumann, K., Kumar, V., Dennier, T., Lyck, R., … Stein,
J. (2011). In vivo analysis of uropod function during physiological T cell trafficking.
Journal of Immunology. American Association of Immunologists. https://doi.org/10.4049/jimmunol.1100935
chicago: Soriano, Silvia, Miroslav Hons, Kathrin Schumann, Varsha Kumar, Timo Dennier,
Ruth Lyck, Michael K Sixt, and Jens Stein. “In Vivo Analysis of Uropod Function
during Physiological T Cell Trafficking.” Journal of Immunology. American
Association of Immunologists, 2011. https://doi.org/10.4049/jimmunol.1100935.
ieee: S. Soriano et al., “In vivo analysis of uropod function during physiological
T cell trafficking,” Journal of Immunology, vol. 187, no. 5. American Association
of Immunologists, pp. 2356–2364, 2011.
ista: Soriano S, Hons M, Schumann K, Kumar V, Dennier T, Lyck R, Sixt MK, Stein
J. 2011. In vivo analysis of uropod function during physiological T cell trafficking.
Journal of Immunology. 187(5), 2356–2364.
mla: Soriano, Silvia, et al. “In Vivo Analysis of Uropod Function during Physiological
T Cell Trafficking.” Journal of Immunology, vol. 187, no. 5, American Association
of Immunologists, 2011, pp. 2356–64, doi:10.4049/jimmunol.1100935.
short: S. Soriano, M. Hons, K. Schumann, V. Kumar, T. Dennier, R. Lyck, M.K. Sixt,
J. Stein, Journal of Immunology 187 (2011) 2356–2364.
date_created: 2018-12-11T12:03:04Z
date_published: 2011-09-01T00:00:00Z
date_updated: 2025-09-30T08:43:55Z
day: '01'
department:
- _id: MiSi
doi: 10.4049/jimmunol.1100935
external_id:
isi:
- '000294059500040'
fulldoi: https://doi.org/10.4049/jimmunol.1100935
intvolume: ' 187'
isi: 1
issue: '5'
language:
- iso: eng
month: '09'
oa_version: None
page: 2356 - 2364
publication: Journal of Immunology
publication_identifier:
eissn:
- 1550-6606
issn:
- 0022-1767
publication_status: published
publisher: American Association of Immunologists
publist_id: '3215'
quality_controlled: '1'
scopus_import: '1'
status: public
title: In vivo analysis of uropod function during physiological T cell trafficking
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 187
year: '2011'
...
---
_id: '3505'
abstract:
- lang: eng
text: Cell migration on two-dimensional (2D) substrates follows entirely different
rules than cell migration in three-dimensional (3D) environments. This is especially
relevant for leukocytes that are able to migrate in the absence of adhesion receptors
within the confined geometry of artificial 3D extracellular matrix scaffolds and
within the interstitial space in vivo. Here, we describe in detail a simple and
economical protocol to visualize dendritic cell migration in 3D collagen scaffolds
along chemotactic gradients. This method can be adapted to other cell types and
may serve as a physiologically relevant paradigm for the directed locomotion of
most amoeboid cells.
alternative_title:
- Methods in Molecular Biology
article_processing_charge: No
article_type: original
author:
- 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: Tim
full_name: Lämmermann, Tim
last_name: Lämmermann
citation:
ama: Sixt MK, Lämmermann T. In vitro analysis of chemotactic leukocyte migration
in 3D environments. Cell Migration. 2011;769:149-165. doi:10.1007/978-1-61779-207-6_11
apa: Sixt, M. K., & Lämmermann, T. (2011). In vitro analysis of chemotactic
leukocyte migration in 3D environments. Cell Migration. Springer. https://doi.org/10.1007/978-1-61779-207-6_11
chicago: Sixt, Michael K, and Tim Lämmermann. “In Vitro Analysis of Chemotactic
Leukocyte Migration in 3D Environments.” Cell Migration. Springer, 2011.
https://doi.org/10.1007/978-1-61779-207-6_11.
ieee: M. K. Sixt and T. Lämmermann, “In vitro analysis of chemotactic leukocyte
migration in 3D environments,” Cell Migration, vol. 769. Springer, pp.
149–165, 2011.
ista: Sixt MK, Lämmermann T. 2011. In vitro analysis of chemotactic leukocyte migration
in 3D environments. Cell Migration. 769, 149–165.
mla: Sixt, Michael K., and Tim Lämmermann. “In Vitro Analysis of Chemotactic Leukocyte
Migration in 3D Environments.” Cell Migration, vol. 769, Springer, 2011,
pp. 149–65, doi:10.1007/978-1-61779-207-6_11.
short: M.K. Sixt, T. Lämmermann, Cell Migration 769 (2011) 149–165.
corr_author: '1'
date_created: 2018-12-11T12:03:41Z
date_published: 2011-05-17T00:00:00Z
date_updated: 2026-06-18T18:46:10Z
day: '17'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1007/978-1-61779-207-6_11
fulldoi: https://doi.org/10.1007/978-1-61779-207-6_11
intvolume: ' 769'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://pure.mpg.de/pubman/item/item_3219628_1/component/file_3219630/Sixt%20et%20al..pdf
month: '05'
oa: 1
oa_version: Published Version
page: 149 - 165
publication: Cell Migration
publication_status: published
publisher: Springer
publist_id: '2882'
quality_controlled: '1'
scopus_import: '1'
status: public
title: In vitro analysis of chemotactic leukocyte migration in 3D environments
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 769
year: '2011'
...