---
_id: '6891'
abstract:
- lang: eng
  text: "While cells of mesenchymal or epithelial origin perform their effector functions
    in a purely anchorage dependent manner, cells derived from the hematopoietic lineage
    are not committed to operate only within a specific niche. Instead, these cells
    are able to function autonomously of the molecular composition in a broad range
    of tissue compartments. By this means, cells of the hematopoietic lineage retain
    the capacity to disseminate into connective tissue and recirculate between organs,
    building the foundation for essential processes such as tissue regeneration or
    immune surveillance. \r\nCells of the immune system, specifically leukocytes,
    are extraordinarily good at performing this task. These cells are able to flexibly
    shift their mode of migration between an adhesion-mediated and an adhesion-independent
    manner, instantaneously accommodating for any changes in molecular composition
    of the external scaffold. The key component driving directed leukocyte migration
    is the chemokine receptor 7, which guides the cell along gradients of chemokine
    ligand. Therefore, the physical destination of migrating leukocytes is purely
    deterministic, i.e. given by global directional cues such as chemokine gradients.
    \r\nNevertheless, these cells typically reside in three-dimensional scaffolds
    of inhomogeneous complexity, raising the question whether cells are able to locally
    discriminate between multiple optional migration routes. Current literature provides
    evidence that leukocytes, specifically dendritic cells, do indeed probe their
    surrounding by virtue of multiple explorative protrusions. However, it remains
    enigmatic how these cells decide which one is the more favorable route to follow
    and what are the key players involved in performing this task. Due to the heterogeneous
    environment of most tissues, and the vast adaptability of migrating leukocytes,
    at this time it is not clear to what extent leukocytes are able to optimize their
    migratory strategy by adapting their level of adhesiveness. And, given the fact
    that leukocyte migration is characterized by branched cell shapes in combination
    with high migration velocities, it is reasonable to assume that these cells require
    fine tuned shape maintenance mechanisms that tightly coordinate protrusion and
    adhesion dynamics in a spatiotemporal manner. \r\nTherefore, this study aimed
    to elucidate how rapidly migrating leukocytes opt for an ideal migratory path
    while maintaining a continuous cell shape and balancing adhesive forces to efficiently
    navigate through complex microenvironments. \r\nThe results of this study unraveled
    a role for the microtubule cytoskeleton in promoting the decision making process
    during path finding and for the first time point towards a microtubule-mediated
    function in cell shape maintenance of highly ramified cells such as dendritic
    cells. Furthermore, we found that migrating low-adhesive leukocytes are able to
    instantaneously adapt to increased tensile load by engaging adhesion receptors.
    This response was only occurring tangential to the substrate while adhesive properties
    in the vertical direction were not increased. As leukocytes are primed for rapid
    migration velocities, these results demonstrate that leukocyte integrins are able
    to confer a high level of traction forces parallel to the cell membrane along
    the direction of migration without wasting energy in gluing the cell to the substrate.
    \r\nThus, the data in the here presented thesis provide new insights into the
    pivotal role of cytoskeletal dynamics and the mechanisms of force transduction
    during leukocyte migration. \r\nThereby the here presented results help to further
    define fundamental principles underlying leukocyte migration and open up potential
    therapeutic avenues of clinical relevance.\r\n"
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Aglaja
  full_name: Kopf, Aglaja
  id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87
  last_name: Kopf
  orcid: 0000-0002-2187-6656
citation:
  ama: Kopf A. The implication of cytoskeletal dynamics on leukocyte migration. 2019.
    doi:<a href="https://doi.org/10.15479/AT:ISTA:6891">10.15479/AT:ISTA:6891</a>
  apa: Kopf, A. (2019). <i>The implication of cytoskeletal dynamics on leukocyte migration</i>.
    Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:6891">https://doi.org/10.15479/AT:ISTA:6891</a>
  chicago: Kopf, Aglaja. “The Implication of Cytoskeletal Dynamics on Leukocyte Migration.”
    Institute of Science and Technology Austria, 2019. <a href="https://doi.org/10.15479/AT:ISTA:6891">https://doi.org/10.15479/AT:ISTA:6891</a>.
  ieee: A. Kopf, “The implication of cytoskeletal dynamics on leukocyte migration,”
    Institute of Science and Technology Austria, 2019.
  ista: Kopf A. 2019. The implication of cytoskeletal dynamics on leukocyte migration.
    Institute of Science and Technology Austria.
  mla: Kopf, Aglaja. <i>The Implication of Cytoskeletal Dynamics on Leukocyte Migration</i>.
    Institute of Science and Technology Austria, 2019, doi:<a href="https://doi.org/10.15479/AT:ISTA:6891">10.15479/AT:ISTA:6891</a>.
  short: A. Kopf, The Implication of Cytoskeletal Dynamics on Leukocyte Migration,
    Institute of Science and Technology Austria, 2019.
date_created: 2019-09-19T08:19:44Z
date_published: 2019-07-24T00:00:00Z
date_updated: 2023-10-18T08:49:17Z
day: '24'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:6891
file:
- access_level: closed
  checksum: 00d100d6468e31e583051e0a006b640c
  content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
  creator: akopf
  date_created: 2019-10-15T05:28:42Z
  date_updated: 2020-10-17T22:30:03Z
  embargo_to: open_access
  file_id: '6950'
  file_name: Kopf_PhD_Thesis.docx
  file_size: 74735267
  relation: source_file
- access_level: open_access
  checksum: 5d1baa899993ae6ca81aebebe1797000
  content_type: application/pdf
  creator: akopf
  date_created: 2019-10-15T05:28:47Z
  date_updated: 2020-10-17T22:30:03Z
  embargo: 2020-10-16
  file_id: '6951'
  file_name: Kopf_PhD_Thesis1.pdf
  file_size: 52787224
  relation: main_file
file_date_updated: 2020-10-17T22:30:03Z
has_accepted_license: '1'
keyword:
- cell biology
- immunology
- leukocyte
- migration
- microfluidics
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: '171'
project:
- _id: 265E2996-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: W01250-B20
  name: Nano-Analytics of Cellular Systems
publication_identifier:
  eissn:
  - 2663-337X
  isbn:
  - 978-3-99078-002-2
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
  link:
  - relation: press_release
    url: https://ist.ac.at/en/news/feeling-like-a-cell/
  record:
  - id: '6328'
    relation: part_of_dissertation
    status: public
  - id: '15'
    relation: part_of_dissertation
    status: public
  - id: '6877'
    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: The implication of cytoskeletal dynamics on leukocyte migration
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2019'
...
---
_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:<a href="https://doi.org/10.15479/AT:ISTA:6947">10.15479/AT:ISTA:6947</a>'
  apa: 'Assen, F. P. (2019). <i>Lymph node mechanics: Deciphering the interplay between
    stroma contractility, morphology and lymphocyte trafficking</i>. Institute of
    Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:6947">https://doi.org/10.15479/AT:ISTA:6947</a>'
  chicago: 'Assen, Frank P. “Lymph Node Mechanics: Deciphering the Interplay between
    Stroma Contractility, Morphology and Lymphocyte Trafficking.” Institute of Science
    and Technology Austria, 2019. <a href="https://doi.org/10.15479/AT:ISTA:6947">https://doi.org/10.15479/AT:ISTA:6947</a>.'
  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. <i>Lymph Node Mechanics: Deciphering the Interplay between
    Stroma Contractility, Morphology and Lymphocyte Trafficking</i>. Institute of
    Science and Technology Austria, 2019, doi:<a href="https://doi.org/10.15479/AT:ISTA:6947">10.15479/AT:ISTA:6947</a>.'
  short: 'F.P. Assen, Lymph Node Mechanics: Deciphering the Interplay between Stroma
    Contractility, Morphology and Lymphocyte Trafficking, Institute of Science and
    Technology Austria, 2019.'
date_created: 2019-10-14T16:54:52Z
date_published: 2019-10-09T00:00:00Z
date_updated: 2023-09-13T08:50:57Z
day: '9'
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
- access_level: open_access
  checksum: 8c156b65d9347bb599623a4b09f15d15
  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: '664'
    relation: part_of_dissertation
    status: public
  - id: '402'
    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: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2019'
...
---
_id: '6979'
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. Gut homeostasis: Active migration of intestinal epithelial
    cells in tissue renewal. <i>Current Biology</i>. 2019;29(20):R1091-R1093. doi:<a
    href="https://doi.org/10.1016/j.cub.2019.08.068">10.1016/j.cub.2019.08.068</a>'
  apa: 'Kopf, A., &#38; Sixt, M. K. (2019). Gut homeostasis: Active migration of intestinal
    epithelial cells in tissue renewal. <i>Current Biology</i>. Cell Press. <a href="https://doi.org/10.1016/j.cub.2019.08.068">https://doi.org/10.1016/j.cub.2019.08.068</a>'
  chicago: 'Kopf, Aglaja, and Michael K Sixt. “Gut Homeostasis: Active Migration of
    Intestinal Epithelial Cells in Tissue Renewal.” <i>Current Biology</i>. Cell Press,
    2019. <a href="https://doi.org/10.1016/j.cub.2019.08.068">https://doi.org/10.1016/j.cub.2019.08.068</a>.'
  ieee: 'A. Kopf and M. K. Sixt, “Gut homeostasis: Active migration of intestinal
    epithelial cells in tissue renewal,” <i>Current Biology</i>, vol. 29, no. 20.
    Cell Press, pp. R1091–R1093, 2019.'
  ista: 'Kopf A, Sixt MK. 2019. Gut homeostasis: Active migration of intestinal epithelial
    cells in tissue renewal. Current Biology. 29(20), R1091–R1093.'
  mla: 'Kopf, Aglaja, and Michael K. Sixt. “Gut Homeostasis: Active Migration of Intestinal
    Epithelial Cells in Tissue Renewal.” <i>Current Biology</i>, vol. 29, no. 20,
    Cell Press, 2019, pp. R1091–93, doi:<a href="https://doi.org/10.1016/j.cub.2019.08.068">10.1016/j.cub.2019.08.068</a>.'
  short: A. Kopf, M.K. Sixt, Current Biology 29 (2019) R1091–R1093.
date_created: 2019-11-04T15:18:29Z
date_published: 2019-10-21T00:00:00Z
date_updated: 2023-09-05T12:43:43Z
day: '21'
department:
- _id: MiSi
doi: 10.1016/j.cub.2019.08.068
external_id:
  isi:
  - '000491286200016'
  pmid:
  - '31639357'
intvolume: '        29'
isi: 1
issue: '20'
language:
- iso: eng
month: '10'
oa_version: None
page: R1091-R1093
pmid: 1
publication: Current Biology
publication_identifier:
  eissn:
  - 1879-0445
  issn:
  - 0960-9822
publication_status: published
publisher: Cell Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Gut homeostasis: Active migration of intestinal epithelial cells in tissue
  renewal'
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 29
year: '2019'
...
---
_id: '6988'
abstract:
- lang: eng
  text: 'Platelets are central players in thrombosis and hemostasis but are increasingly
    recognized as key components of the immune system. They shape ensuing immune responses
    by recruiting leukocytes, and support the development of adaptive immunity. Recent
    data shed new light on the complex role of platelets in immunity. Here, we summarize
    experimental and clinical data on the role of platelets in host defense against
    bacteria. Platelets bind, contain, and kill bacteria directly; however, platelet
    proinflammatory effector functions and cross-talk with the coagulation system,
    can also result in damage to the host (e.g., acute lung injury and sepsis). Novel
    clinical insights support this dichotomy: platelet inhibition/thrombocytopenia
    can be either harmful or protective, depending on pathophysiological context.
    Clinical studies are currently addressing this aspect in greater depth.'
article_processing_charge: No
article_type: review
author:
- first_name: Leo
  full_name: Nicolai, Leo
  last_name: Nicolai
- 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: Steffen
  full_name: Massberg, Steffen
  last_name: Massberg
citation:
  ama: 'Nicolai L, Gärtner FR, Massberg S. Platelets in host defense: Experimental
    and clinical insights. <i>Trends in Immunology</i>. 2019;40(10):922-938. doi:<a
    href="https://doi.org/10.1016/j.it.2019.08.004">10.1016/j.it.2019.08.004</a>'
  apa: 'Nicolai, L., Gärtner, F. R., &#38; Massberg, S. (2019). Platelets in host
    defense: Experimental and clinical insights. <i>Trends in Immunology</i>. Cell
    Press. <a href="https://doi.org/10.1016/j.it.2019.08.004">https://doi.org/10.1016/j.it.2019.08.004</a>'
  chicago: 'Nicolai, Leo, Florian R Gärtner, and Steffen Massberg. “Platelets in Host
    Defense: Experimental and Clinical Insights.” <i>Trends in Immunology</i>. Cell
    Press, 2019. <a href="https://doi.org/10.1016/j.it.2019.08.004">https://doi.org/10.1016/j.it.2019.08.004</a>.'
  ieee: 'L. Nicolai, F. R. Gärtner, and S. Massberg, “Platelets in host defense: Experimental
    and clinical insights,” <i>Trends in Immunology</i>, vol. 40, no. 10. Cell Press,
    pp. 922–938, 2019.'
  ista: 'Nicolai L, Gärtner FR, Massberg S. 2019. Platelets in host defense: Experimental
    and clinical insights. Trends in Immunology. 40(10), 922–938.'
  mla: 'Nicolai, Leo, et al. “Platelets in Host Defense: Experimental and Clinical
    Insights.” <i>Trends in Immunology</i>, vol. 40, no. 10, Cell Press, 2019, pp.
    922–38, doi:<a href="https://doi.org/10.1016/j.it.2019.08.004">10.1016/j.it.2019.08.004</a>.'
  short: L. Nicolai, F.R. Gärtner, S. Massberg, Trends in Immunology 40 (2019) 922–938.
date_created: 2019-11-04T16:27:36Z
date_published: 2019-10-01T00:00:00Z
date_updated: 2023-08-30T07:19:23Z
day: '01'
department:
- _id: MiSi
doi: 10.1016/j.it.2019.08.004
ec_funded: 1
external_id:
  isi:
  - '000493292100005'
  pmid:
  - '31601520'
intvolume: '        40'
isi: 1
issue: '10'
language:
- iso: eng
month: '10'
oa_version: None
page: 922-938
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: Trends in Immunology
publication_identifier:
  issn:
  - 1471-4906
publication_status: published
publisher: Cell Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Platelets in host defense: Experimental and clinical insights'
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 40
year: '2019'
...
---
_id: '7009'
abstract:
- lang: eng
  text: Cell migration is essential for physiological processes as diverse as development,
    immune defence and wound healing. It is also a hallmark of cancer malignancy.
    Thousands of publications have elucidated detailed molecular and biophysical mechanisms
    of cultured cells migrating on flat, 2D substrates of glass and plastic. However,
    much less is known about how cells successfully navigate the complex 3D environments
    of living tissues. In these more complex, native environments, cells use multiple
    modes of migration, including mesenchymal, amoeboid, lobopodial and collective,
    and these are governed by the local extracellular microenvironment, specific modalities
    of Rho GTPase signalling and non- muscle myosin contractility. Migration through
    3D environments is challenging because it requires the cell to squeeze through
    complex or dense extracellular structures. Doing so requires specific cellular
    adaptations to mechanical features of the extracellular matrix (ECM) or its remodelling.
    In addition, besides navigating through diverse ECM environments and overcoming
    extracellular barriers, cells often interact with neighbouring cells and tissues
    through physical and signalling interactions. Accordingly, cells need to call
    on an impressively wide diversity of mechanisms to meet these challenges. This
    Review examines how cells use both classical and novel mechanisms of locomotion
    as they traverse challenging 3D matrices and cellular environments. It focuses
    on principles rather than details of migratory mechanisms and draws comparisons
    between 1D, 2D and 3D migration.
article_processing_charge: No
article_type: review
author:
- first_name: KM
  full_name: Yamada, KM
  last_name: Yamada
- 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: Yamada K, Sixt MK. Mechanisms of 3D cell migration. <i>Nature Reviews Molecular
    Cell Biology</i>. 2019;20(12):738–752. doi:<a href="https://doi.org/10.1038/s41580-019-0172-9">10.1038/s41580-019-0172-9</a>
  apa: Yamada, K., &#38; Sixt, M. K. (2019). Mechanisms of 3D cell migration. <i>Nature
    Reviews Molecular Cell Biology</i>. Springer Nature. <a href="https://doi.org/10.1038/s41580-019-0172-9">https://doi.org/10.1038/s41580-019-0172-9</a>
  chicago: Yamada, KM, and Michael K Sixt. “Mechanisms of 3D Cell Migration.” <i>Nature
    Reviews Molecular Cell Biology</i>. Springer Nature, 2019. <a href="https://doi.org/10.1038/s41580-019-0172-9">https://doi.org/10.1038/s41580-019-0172-9</a>.
  ieee: K. Yamada and M. K. Sixt, “Mechanisms of 3D cell migration,” <i>Nature Reviews
    Molecular Cell Biology</i>, vol. 20, no. 12. Springer Nature, pp. 738–752, 2019.
  ista: Yamada K, Sixt MK. 2019. Mechanisms of 3D cell migration. Nature Reviews Molecular
    Cell Biology. 20(12), 738–752.
  mla: Yamada, KM, and Michael K. Sixt. “Mechanisms of 3D Cell Migration.” <i>Nature
    Reviews Molecular Cell Biology</i>, vol. 20, no. 12, Springer Nature, 2019, pp.
    738–752, doi:<a href="https://doi.org/10.1038/s41580-019-0172-9">10.1038/s41580-019-0172-9</a>.
  short: K. Yamada, M.K. Sixt, Nature Reviews Molecular Cell Biology 20 (2019) 738–752.
date_created: 2019-11-12T14:54:42Z
date_published: 2019-12-01T00:00:00Z
date_updated: 2023-08-30T07:22:20Z
day: '01'
department:
- _id: MiSi
doi: 10.1038/s41580-019-0172-9
external_id:
  isi:
  - '000497966900007'
  pmid:
  - '31582855'
intvolume: '        20'
isi: 1
issue: '12'
language:
- iso: eng
month: '12'
oa_version: None
page: 738–752
pmid: 1
publication: Nature Reviews Molecular Cell Biology
publication_identifier:
  eissn:
  - 1471-0080
  issn:
  - 1471-0072
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mechanisms of 3D cell migration
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 20
year: '2019'
...
---
_id: '7105'
abstract:
- lang: eng
  text: Cell migration is hypothesized to involve a cycle of behaviours beginning
    with leading edge extension. However, recent evidence suggests that the leading
    edge may be dispensable for migration, raising the question of what actually controls
    cell directionality. Here, we exploit the embryonic migration of Drosophila macrophages
    to bridge the different temporal scales of the behaviours controlling motility.
    This approach reveals that edge fluctuations during random motility are not persistent
    and are weakly correlated with motion. In contrast, flow of the actin network
    behind the leading edge is highly persistent. Quantification of actin flow structure
    during migration reveals a stable organization and asymmetry in the cell-wide
    flowfield that strongly correlates with cell directionality. This organization
    is regulated by a gradient of actin network compression and destruction, which
    is controlled by myosin contraction and cofilin-mediated disassembly. It is this
    stable actin-flow polarity, which integrates rapid fluctuations of the leading
    edge, that controls inherent cellular persistence.
article_processing_charge: No
article_type: original
author:
- first_name: Lawrence
  full_name: Yolland, Lawrence
  last_name: Yolland
- first_name: Mubarik
  full_name: Burki, Mubarik
  last_name: Burki
- first_name: Stefania
  full_name: Marcotti, Stefania
  last_name: Marcotti
- first_name: Andrei
  full_name: Luchici, Andrei
  last_name: Luchici
- first_name: Fiona N.
  full_name: Kenny, Fiona N.
  last_name: Kenny
- first_name: John Robert
  full_name: Davis, John Robert
  last_name: Davis
- first_name: Eduardo
  full_name: Serna-Morales, Eduardo
  last_name: Serna-Morales
- 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
- first_name: Andrew
  full_name: Davidson, Andrew
  last_name: Davidson
- first_name: Will
  full_name: Wood, Will
  last_name: Wood
- first_name: Linus J.
  full_name: Schumacher, Linus J.
  last_name: Schumacher
- first_name: Robert G.
  full_name: Endres, Robert G.
  last_name: Endres
- first_name: Mark
  full_name: Miodownik, Mark
  last_name: Miodownik
- first_name: Brian M.
  full_name: Stramer, Brian M.
  last_name: Stramer
citation:
  ama: Yolland L, Burki M, Marcotti S, et al. Persistent and polarized global actin
    flow is essential for directionality during cell migration. <i>Nature Cell Biology</i>.
    2019;21(11):1370-1381. doi:<a href="https://doi.org/10.1038/s41556-019-0411-5">10.1038/s41556-019-0411-5</a>
  apa: Yolland, L., Burki, M., Marcotti, S., Luchici, A., Kenny, F. N., Davis, J.
    R., … Stramer, B. M. (2019). Persistent and polarized global actin flow is essential
    for directionality during cell migration. <i>Nature Cell Biology</i>. Springer
    Nature. <a href="https://doi.org/10.1038/s41556-019-0411-5">https://doi.org/10.1038/s41556-019-0411-5</a>
  chicago: Yolland, Lawrence, Mubarik Burki, Stefania Marcotti, Andrei Luchici, Fiona
    N. Kenny, John Robert Davis, Eduardo Serna-Morales, et al. “Persistent and Polarized
    Global Actin Flow Is Essential for Directionality during Cell Migration.” <i>Nature
    Cell Biology</i>. Springer Nature, 2019. <a href="https://doi.org/10.1038/s41556-019-0411-5">https://doi.org/10.1038/s41556-019-0411-5</a>.
  ieee: L. Yolland <i>et al.</i>, “Persistent and polarized global actin flow is essential
    for directionality during cell migration,” <i>Nature Cell Biology</i>, vol. 21,
    no. 11. Springer Nature, pp. 1370–1381, 2019.
  ista: Yolland L, Burki M, Marcotti S, Luchici A, Kenny FN, Davis JR, Serna-Morales
    E, Müller J, Sixt MK, Davidson A, Wood W, Schumacher LJ, Endres RG, Miodownik
    M, Stramer BM. 2019. Persistent and polarized global actin flow is essential for
    directionality during cell migration. Nature Cell Biology. 21(11), 1370–1381.
  mla: Yolland, Lawrence, et al. “Persistent and Polarized Global Actin Flow Is Essential
    for Directionality during Cell Migration.” <i>Nature Cell Biology</i>, vol. 21,
    no. 11, Springer Nature, 2019, pp. 1370–81, doi:<a href="https://doi.org/10.1038/s41556-019-0411-5">10.1038/s41556-019-0411-5</a>.
  short: L. Yolland, M. Burki, S. Marcotti, A. Luchici, F.N. Kenny, J.R. Davis, E.
    Serna-Morales, J. Müller, M.K. Sixt, A. Davidson, W. Wood, L.J. Schumacher, R.G.
    Endres, M. Miodownik, B.M. Stramer, Nature Cell Biology 21 (2019) 1370–1381.
date_created: 2019-11-25T08:55:00Z
date_published: 2019-11-01T00:00:00Z
date_updated: 2023-09-06T11:08:52Z
day: '01'
department:
- _id: MiSi
doi: 10.1038/s41556-019-0411-5
external_id:
  isi:
  - '000495888300009'
  pmid:
  - '31685997'
intvolume: '        21'
isi: 1
issue: '11'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7025891
month: '11'
oa: 1
oa_version: Submitted Version
page: 1370-1381
pmid: 1
publication: Nature Cell Biology
publication_identifier:
  eissn:
  - 1476-4679
  issn:
  - 1465-7392
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Persistent and polarized global actin flow is essential for directionality
  during cell migration
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 21
year: '2019'
...
---
_id: '7404'
abstract:
- lang: eng
  text: The formation of neuronal dendrite branches is fundamental for the wiring
    and function of the nervous system. Indeed, dendrite branching enhances the coverage
    of the neuron's receptive field and modulates the initial processing of incoming
    stimuli. Complex dendrite patterns are achieved in vivo through a dynamic process
    of de novo branch formation, branch extension and retraction. The first step towards
    branch formation is the generation of a dynamic filopodium-like branchlet. The
    mechanisms underlying the initiation of dendrite branchlets are therefore crucial
    to the shaping of dendrites. Through in vivo time-lapse imaging of the subcellular
    localization of actin during the process of branching of Drosophila larva sensory
    neurons, combined with genetic analysis and electron tomography, we have identified
    the Actin-related protein (Arp) 2/3 complex as the major actin nucleator involved
    in the initiation of dendrite branchlet formation, under the control of the activator
    WAVE and of the small GTPase Rac1. Transient recruitment of an Arp2/3 component
    marks the site of branchlet initiation in vivo. These data position the activation
    of Arp2/3 as an early hub for the initiation of branchlet formation.
article_number: dev171397
article_processing_charge: No
article_type: original
author:
- first_name: Tomke
  full_name: Stürner, Tomke
  last_name: Stürner
- first_name: Anastasia
  full_name: Tatarnikova, Anastasia
  last_name: Tatarnikova
- first_name: Jan
  full_name: Müller, Jan
  id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
  last_name: Müller
- first_name: Barbara
  full_name: Schaffran, Barbara
  last_name: Schaffran
- first_name: Hermann
  full_name: Cuntz, Hermann
  last_name: Cuntz
- first_name: Yun
  full_name: Zhang, Yun
  last_name: Zhang
- first_name: Maria
  full_name: Nemethova, Maria
  id: 34E27F1C-F248-11E8-B48F-1D18A9856A87
  last_name: Nemethova
- first_name: Sven
  full_name: Bogdan, Sven
  last_name: Bogdan
- first_name: Vic
  full_name: Small, Vic
  last_name: Small
- first_name: Gaia
  full_name: Tavosanis, Gaia
  last_name: Tavosanis
citation:
  ama: Stürner T, Tatarnikova A, Müller J, et al. Transient localization of the Arp2/3
    complex initiates neuronal dendrite branching in vivo. <i>Development</i>. 2019;146(7).
    doi:<a href="https://doi.org/10.1242/dev.171397">10.1242/dev.171397</a>
  apa: Stürner, T., Tatarnikova, A., Müller, J., Schaffran, B., Cuntz, H., Zhang,
    Y., … Tavosanis, G. (2019). Transient localization of the Arp2/3 complex initiates
    neuronal dendrite branching in vivo. <i>Development</i>. The Company of Biologists.
    <a href="https://doi.org/10.1242/dev.171397">https://doi.org/10.1242/dev.171397</a>
  chicago: Stürner, Tomke, Anastasia Tatarnikova, Jan Müller, Barbara Schaffran, Hermann
    Cuntz, Yun Zhang, Maria Nemethova, Sven Bogdan, Vic Small, and Gaia Tavosanis.
    “Transient Localization of the Arp2/3 Complex Initiates Neuronal Dendrite Branching
    in Vivo.” <i>Development</i>. The Company of Biologists, 2019. <a href="https://doi.org/10.1242/dev.171397">https://doi.org/10.1242/dev.171397</a>.
  ieee: T. Stürner <i>et al.</i>, “Transient localization of the Arp2/3 complex initiates
    neuronal dendrite branching in vivo,” <i>Development</i>, vol. 146, no. 7. The
    Company of Biologists, 2019.
  ista: Stürner T, Tatarnikova A, Müller J, Schaffran B, Cuntz H, Zhang Y, Nemethova
    M, Bogdan S, Small V, Tavosanis G. 2019. Transient localization of the Arp2/3
    complex initiates neuronal dendrite branching in vivo. Development. 146(7), dev171397.
  mla: Stürner, Tomke, et al. “Transient Localization of the Arp2/3 Complex Initiates
    Neuronal Dendrite Branching in Vivo.” <i>Development</i>, vol. 146, no. 7, dev171397,
    The Company of Biologists, 2019, doi:<a href="https://doi.org/10.1242/dev.171397">10.1242/dev.171397</a>.
  short: T. Stürner, A. Tatarnikova, J. Müller, B. Schaffran, H. Cuntz, Y. Zhang,
    M. Nemethova, S. Bogdan, V. Small, G. Tavosanis, Development 146 (2019).
date_created: 2020-01-29T16:27:10Z
date_published: 2019-04-04T00:00:00Z
date_updated: 2023-09-07T14:47:00Z
day: '04'
department:
- _id: MiSi
doi: 10.1242/dev.171397
external_id:
  isi:
  - '000464583200006'
  pmid:
  - '30910826'
intvolume: '       146'
isi: 1
issue: '7'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1242/dev.171397
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
publication: Development
publication_identifier:
  eissn:
  - 1477-9129
  issn:
  - 0950-1991
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
scopus_import: '1'
status: public
title: Transient localization of the Arp2/3 complex initiates neuronal dendrite branching
  in vivo
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 146
year: '2019'
...
---
_id: '7420'
abstract:
- lang: eng
  text: β1-integrins mediate cell–matrix interactions and their trafficking is important
    in the dynamic regulation of cell adhesion, migration and malignant processes,
    including cancer cell invasion. Here, we employ an RNAi screen to characterize
    regulators of integrin traffic and identify the association of Golgi-localized
    gamma ear-containing Arf-binding protein 2 (GGA2) with β1-integrin, and its role
    in recycling of active but not inactive β1-integrin receptors. Silencing of GGA2
    limits active β1-integrin levels in focal adhesions and decreases cancer cell
    migration and invasion, which is in agreement with its ability to regulate the
    dynamics of active integrins. By using the proximity-dependent biotin identification
    (BioID) method, we identified two RAB family small GTPases, i.e. RAB13 and RAB10,
    as novel interactors of GGA2. Functionally, RAB13 silencing triggers the intracellular
    accumulation of active β1-integrin, and reduces integrin activity in focal adhesions
    and cell migration similarly to GGA2 depletion, indicating that both facilitate
    active β1-integrin recycling to the plasma membrane. Thus, GGA2 and RAB13 are
    important specificity determinants for integrin activity-dependent traffic.
article_number: jcs233387
article_processing_charge: No
article_type: original
author:
- first_name: Pranshu
  full_name: Sahgal, Pranshu
  last_name: Sahgal
- 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: Jaroslav
  full_name: Icha, Jaroslav
  last_name: Icha
- first_name: Ilkka
  full_name: Paatero, Ilkka
  last_name: Paatero
- first_name: Hellyeh
  full_name: Hamidi, Hellyeh
  last_name: Hamidi
- first_name: Antti
  full_name: Arjonen, Antti
  last_name: Arjonen
- first_name: Mika
  full_name: Pietilä, Mika
  last_name: Pietilä
- first_name: Anne
  full_name: Rokka, Anne
  last_name: Rokka
- first_name: Johanna
  full_name: Ivaska, Johanna
  last_name: Ivaska
citation:
  ama: Sahgal P, Alanko JH, Icha J, et al. GGA2 and RAB13 promote activity-dependent
    β1-integrin recycling. <i>Journal of Cell Science</i>. 2019;132(11). doi:<a href="https://doi.org/10.1242/jcs.233387">10.1242/jcs.233387</a>
  apa: Sahgal, P., Alanko, J. H., Icha, J., Paatero, I., Hamidi, H., Arjonen, A.,
    … Ivaska, J. (2019). GGA2 and RAB13 promote activity-dependent β1-integrin recycling.
    <i>Journal of Cell Science</i>. The Company of Biologists. <a href="https://doi.org/10.1242/jcs.233387">https://doi.org/10.1242/jcs.233387</a>
  chicago: Sahgal, Pranshu, Jonna H Alanko, Jaroslav Icha, Ilkka Paatero, Hellyeh
    Hamidi, Antti Arjonen, Mika Pietilä, Anne Rokka, and Johanna Ivaska. “GGA2 and
    RAB13 Promote Activity-Dependent Β1-Integrin Recycling.” <i>Journal of Cell Science</i>.
    The Company of Biologists, 2019. <a href="https://doi.org/10.1242/jcs.233387">https://doi.org/10.1242/jcs.233387</a>.
  ieee: P. Sahgal <i>et al.</i>, “GGA2 and RAB13 promote activity-dependent β1-integrin
    recycling,” <i>Journal of Cell Science</i>, vol. 132, no. 11. The Company of Biologists,
    2019.
  ista: Sahgal P, Alanko JH, Icha J, Paatero I, Hamidi H, Arjonen A, Pietilä M, Rokka
    A, Ivaska J. 2019. GGA2 and RAB13 promote activity-dependent β1-integrin recycling.
    Journal of Cell Science. 132(11), jcs233387.
  mla: Sahgal, Pranshu, et al. “GGA2 and RAB13 Promote Activity-Dependent Β1-Integrin
    Recycling.” <i>Journal of Cell Science</i>, vol. 132, no. 11, jcs233387, The Company
    of Biologists, 2019, doi:<a href="https://doi.org/10.1242/jcs.233387">10.1242/jcs.233387</a>.
  short: P. Sahgal, J.H. Alanko, J. Icha, I. Paatero, H. Hamidi, A. Arjonen, M. Pietilä,
    A. Rokka, J. Ivaska, Journal of Cell Science 132 (2019).
date_created: 2020-01-30T10:31:42Z
date_published: 2019-06-07T00:00:00Z
date_updated: 2023-09-06T15:01:00Z
day: '07'
department:
- _id: MiSi
doi: 10.1242/jcs.233387
external_id:
  isi:
  - '000473327900017'
  pmid:
  - '31076515'
intvolume: '       132'
isi: 1
issue: '11'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1242/jcs.233387
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
publication: Journal of Cell Science
publication_identifier:
  eissn:
  - 1477-9137
  issn:
  - 0021-9533
publication_status: published
publisher: The Company of Biologists
quality_controlled: '1'
status: public
title: GGA2 and RAB13 promote activity-dependent β1-integrin recycling
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 132
year: '2019'
...
---
_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. <i>Nature</i>. 2019;568:546-550.
    doi:<a href="https://doi.org/10.1038/s41586-019-1087-5">10.1038/s41586-019-1087-5</a>
  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. <i>Nature</i>. Springer Nature. <a href="https://doi.org/10.1038/s41586-019-1087-5">https://doi.org/10.1038/s41586-019-1087-5</a>
  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.” <i>Nature</i>. Springer
    Nature, 2019. <a href="https://doi.org/10.1038/s41586-019-1087-5">https://doi.org/10.1038/s41586-019-1087-5</a>.
  ieee: J. Renkawitz <i>et al.</i>, “Nuclear positioning facilitates amoeboid migration
    along the path of least resistance,” <i>Nature</i>, 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.” <i>Nature</i>, vol. 568, Springer Nature,
    2019, pp. 546–50, doi:<a href="https://doi.org/10.1038/s41586-019-1087-5">10.1038/s41586-019-1087-5</a>.
  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: 2024-03-25T23:30:22Z
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
    (EU)
- _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: '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 &gt; 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. <i>Journal of Cell Biology</i>. 2018;217(6):2205-2221.
    doi:<a href="https://doi.org/10.1083/jcb.201612051">10.1083/jcb.201612051</a>
  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. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a
    href="https://doi.org/10.1083/jcb.201612051">https://doi.org/10.1083/jcb.201612051</a>
  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.” <i>Journal of Cell Biology</i>. Rockefeller University
    Press, 2018. <a href="https://doi.org/10.1083/jcb.201612051">https://doi.org/10.1083/jcb.201612051</a>.
  ieee: M. Brown <i>et al.</i>, “Lymphatic exosomes promote dendritic cell migration
    along guidance cues,” <i>Journal of Cell Biology</i>, 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.” <i>Journal of Cell Biology</i>, vol. 217, no. 6, Rockefeller
    University Press, 2018, pp. 2205–21, doi:<a href="https://doi.org/10.1083/jcb.201612051">10.1083/jcb.201612051</a>.
  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.
date_created: 2018-12-11T11:45:33Z
date_published: 2018-04-12T00:00:00Z
date_updated: 2023-09-13T08:51:29Z
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 transduction of leukocytes (FWF)
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '281556'
  name: Cytoskeletal force generation and force transduction of migrating leukocytes
    (EU)
publication: 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. <i>PLoS One</i>. 2018;13(6). doi:<a href="https://doi.org/10.1371/journal.pone.0198330">10.1371/journal.pone.0198330</a>
  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. <i>PLoS One</i>. Public Library of Science. <a href="https://doi.org/10.1371/journal.pone.0198330">https://doi.org/10.1371/journal.pone.0198330</a>
  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.” <i>PLoS One</i>. Public Library
    of Science, 2018. <a href="https://doi.org/10.1371/journal.pone.0198330">https://doi.org/10.1371/journal.pone.0198330</a>.
  ieee: C. Frick <i>et al.</i>, “Nano-scale microfluidics to study 3D chemotaxis at
    the single cell level,” <i>PLoS One</i>, 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.” <i>PLoS One</i>, vol. 13, no. 6, e0198330, Public Library
    of Science, 2018, doi:<a href="https://doi.org/10.1371/journal.pone.0198330">10.1371/journal.pone.0198330</a>.
  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. <i>Developmental Cell</i>.
    2018;45(3):331-346. doi:<a href="https://doi.org/10.1016/j.devcel.2018.04.002">10.1016/j.devcel.2018.04.002</a>
  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. <i>Developmental Cell</i>. Elsevier.
    <a href="https://doi.org/10.1016/j.devcel.2018.04.002">https://doi.org/10.1016/j.devcel.2018.04.002</a>
  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.” <i>Developmental Cell</i>. Elsevier,
    2018. <a href="https://doi.org/10.1016/j.devcel.2018.04.002">https://doi.org/10.1016/j.devcel.2018.04.002</a>.
  ieee: A. Ratheesh <i>et al.</i>, “Drosophila TNF modulates tissue tension in the
    embryo to facilitate macrophage invasive migration,” <i>Developmental Cell</i>,
    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.” <i>Developmental Cell</i>, vol.
    45, no. 3, Elsevier, 2018, pp. 331–46, doi:<a href="https://doi.org/10.1016/j.devcel.2018.04.002">10.1016/j.devcel.2018.04.002</a>.
  short: A. Ratheesh, J. Bicher, M. Smutny, J. Veselá, E. Papusheva, G. Krens, W.
    Kaufmann, A. György, A.M. Casano, D.E. Siekhaus, Developmental Cell 45 (2018)
    331–346.
date_created: 2018-12-11T11:45:44Z
date_published: 2018-05-07T00:00:00Z
date_updated: 2023-09-11T13:22:13Z
day: '07'
department:
- _id: DaSi
- _id: CaHe
- _id: Bio
- _id: EM-Fac
- _id: MiSi
doi: 10.1016/j.devcel.2018.04.002
ec_funded: 1
external_id:
  isi:
  - '000432461400009'
  pmid:
  - '29738712'
intvolume: '        45'
isi: 1
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1016/j.devcel.2018.04.002
month: '05'
oa: 1
oa_version: Published Version
page: 331 - 346
pmid: 1
project:
- _id: 253B6E48-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P29638
  name: Drosophila TNFa´s Funktion in Immunzellen
- _id: 2536F660-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '334077'
  name: Investigating the role of transporters in invasive migration through junctions
publication: Developmental Cell
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
  link:
  - description: News on IST Homepage
    relation: press_release
    url: https://ist.ac.at/en/news/cells-change-tension-to-make-tissue-barriers-easier-to-get-through/
scopus_import: '1'
status: public
title: Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage
  invasive migration
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 45
year: '2018'
...
---
_id: '318'
abstract:
- lang: eng
  text: The insect’s fat body combines metabolic and immunological functions. In this
    issue of Developmental Cell, Franz et al. (2018) show that in Drosophila, cells
    of the fat body are not static, but can actively “swim” toward sites of epithelial
    injury, where they physically clog the wound and locally secrete antimicrobial
    peptides.
acknowledgement: Short Survey
article_processing_charge: No
author:
- first_name: Alessandra M
  full_name: Casano, Alessandra M
  id: 3DBA3F4E-F248-11E8-B48F-1D18A9856A87
  last_name: Casano
  orcid: 0000-0002-6009-6804
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
citation:
  ama: Casano AM, Sixt MK. A fat lot of good for wound healing. <i>Developmental Cell</i>.
    2018;44(4):405-406. doi:<a href="https://doi.org/10.1016/j.devcel.2018.02.009">10.1016/j.devcel.2018.02.009</a>
  apa: Casano, A. M., &#38; Sixt, M. K. (2018). A fat lot of good for wound healing.
    <i>Developmental Cell</i>. Cell Press. <a href="https://doi.org/10.1016/j.devcel.2018.02.009">https://doi.org/10.1016/j.devcel.2018.02.009</a>
  chicago: Casano, Alessandra M, and Michael K Sixt. “A Fat Lot of Good for Wound
    Healing.” <i>Developmental Cell</i>. Cell Press, 2018. <a href="https://doi.org/10.1016/j.devcel.2018.02.009">https://doi.org/10.1016/j.devcel.2018.02.009</a>.
  ieee: A. M. Casano and M. K. Sixt, “A fat lot of good for wound healing,” <i>Developmental
    Cell</i>, 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.”
    <i>Developmental Cell</i>, vol. 44, no. 4, Cell Press, 2018, pp. 405–06, doi:<a
    href="https://doi.org/10.1016/j.devcel.2018.02.009">10.1016/j.devcel.2018.02.009</a>.
  short: A.M. Casano, M.K. Sixt, Developmental Cell 44 (2018) 405–406.
date_created: 2018-12-11T11:45:47Z
date_published: 2018-02-26T00:00:00Z
date_updated: 2023-09-08T11:42:28Z
day: '26'
department:
- _id: MiSi
doi: 10.1016/j.devcel.2018.02.009
external_id:
  isi:
  - '000426150700002'
  pmid:
  - '29486189'
intvolume: '        44'
isi: 1
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pubmed/29486189
month: '02'
oa: 1
oa_version: Published Version
page: 405 - 406
pmid: 1
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '7547'
quality_controlled: '1'
scopus_import: '1'
status: public
title: A fat lot of good for wound healing
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 44
year: '2018'
...
---
_id: '323'
abstract:
- lang: eng
  text: 'In the here presented thesis, we explore the role of branched actin networks
    in cell migration and antigen presentation, the two most relevant processes in
    dendritic cell biology. Branched actin networks construct lamellipodial protrusions
    at the leading edge of migrating cells. These are typically seen as adhesive structures,
    which mediate force transduction to the extracellular matrix that leads to forward
    locomotion. We ablated Arp2/3 nucleation promoting factor WAVE in DCs and found
    that the resulting cells lack lamellipodial protrusions. Instead, depending on
    the maturation state, one or multiple filopodia were formed. By challenging these
    cells in a variety of migration assays we found that lamellipodial protrusions
    are dispensable for the locomotion of leukocytes and actually dampen the speed
    of migration. However, lamellipodia are critically required to negotiate complex
    environments that DCs experience while they travel to the next draining lymph
    node. Taken together our results suggest that leukocyte lamellipodia have rather
    a sensory- than a force transducing function. Furthermore, we show for the first
    time structure and dynamics of dendritic cell F-actin at the immunological synapse
    with naïve T cells. Dendritic cell F-actin appears as dynamic foci that are nucleated
    by the Arp2/3 complex. WAVE ablated dendritic cells show increased membrane tension,
    leading to an altered ultrastructure of the immunological synapse and severe T
    cell priming defects. These results point towards a previously unappreciated role
    of the cellular mechanics of dendritic cells in T cell activation. Additionally,
    we present a novel cell culture based system for the differentiation of dendritic
    cells from conditionally immortalized hematopoietic precursors. These precursor
    cells are genetically tractable via the CRISPR/Cas9 system while they retain their
    ability to differentiate into highly migratory dendritic cells and other immune
    cells. This will foster the study of all aspects of dendritic cell biology and
    beyond. '
acknowledged_ssus:
- _id: NanoFab
- _id: Bio
- _id: PreCl
- _id: EM-Fac
acknowledgement: "First of all I would like to thank Michael Sixt for giving me the
  opportunity to work in \r\nhis group and for his support throughout the years. He
  is a truly inspiring person and \r\nthe  best  boss  one  can  imagine.  I  would
  \ also  like  to  thank  all  current  and  past \r\nmembers of the Sixt group for
  their help and the great working atmosphere in the lab. \r\nIt is a true privilege
  to work with such a bright, funny and friendly group of people and \r\nI’m  proud
  \ that  I  could  be  part  of  it.  Furthermore,  I  would  like  to  say  ‘thank
  \ you’  to Daria Siekhaus for all the meetings and discussion we had throughout
  the years \r\nand to  Federica  Benvenuti  for  being  part  of  my  committee.
  \ I  am  also  grateful  to  Jack \r\nMerrin  in  the  nanofabrication  facility
  \ and  all  the  people  working  in  the  bioimaging-\r\n, the electron microscopy-
  and the preclinical facilities."
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Alexander F
  full_name: Leithner, Alexander F
  id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
  last_name: Leithner
  orcid: 0000-0002-1073-744X
citation:
  ama: Leithner AF. Branched actin networks in dendritic cell biology. 2018. doi:<a
    href="https://doi.org/10.15479/AT:ISTA:th_998">10.15479/AT:ISTA:th_998</a>
  apa: Leithner, A. F. (2018). <i>Branched actin networks in dendritic cell biology</i>.
    Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:th_998">https://doi.org/10.15479/AT:ISTA:th_998</a>
  chicago: Leithner, Alexander F. “Branched Actin Networks in Dendritic Cell Biology.”
    Institute of Science and Technology Austria, 2018. <a href="https://doi.org/10.15479/AT:ISTA:th_998">https://doi.org/10.15479/AT:ISTA:th_998</a>.
  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. <i>Branched Actin Networks in Dendritic Cell Biology</i>.
    Institute of Science and Technology Austria, 2018, doi:<a href="https://doi.org/10.15479/AT:ISTA:th_998">10.15479/AT:ISTA:th_998</a>.
  short: A.F. Leithner, Branched Actin Networks in Dendritic Cell Biology, Institute
    of Science and Technology Austria, 2018.
date_created: 2018-12-11T11:45:49Z
date_published: 2018-04-12T00:00:00Z
date_updated: 2023-09-07T12:39:44Z
day: '12'
ddc:
- '571'
- '599'
- '610'
degree_awarded: PhD
department:
- _id: MiSi
doi: 10.15479/AT:ISTA:th_998
file:
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  date_created: 2019-04-05T09:23:11Z
  date_updated: 2021-02-11T23:30:17Z
  embargo_to: open_access
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  file_name: PhD_thesis_AlexLeithner_final_version.docx
  file_size: 29027671
  relation: source_file
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  content_type: application/pdf
  creator: dernst
  date_created: 2019-04-05T09:23:11Z
  date_updated: 2021-02-11T11:17:16Z
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  relation: main_file
file_date_updated: 2021-02-11T23:30:17Z
has_accepted_license: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: '99'
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '7542'
pubrep_id: '998'
related_material:
  record:
  - id: '1321'
    relation: part_of_dissertation
    status: public
status: public
supervisor:
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
title: Branched actin networks in dendritic cell biology
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2018'
...
---
_id: '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. <i>Journal of Experimental Medicine</i>.
    2018;215(12):2959-2961. doi:<a href="https://doi.org/10.1084/jem.20181934">10.1084/jem.20181934</a>
  apa: Reversat, A., &#38; Sixt, M. K. (2018). IgM’s exit route. <i>Journal of Experimental
    Medicine</i>. Rockefeller University Press. <a href="https://doi.org/10.1084/jem.20181934">https://doi.org/10.1084/jem.20181934</a>
  chicago: Reversat, Anne, and Michael K Sixt. “IgM’s Exit Route.” <i>Journal of Experimental
    Medicine</i>. Rockefeller University Press, 2018. <a href="https://doi.org/10.1084/jem.20181934">https://doi.org/10.1084/jem.20181934</a>.
  ieee: A. Reversat and M. K. Sixt, “IgM’s exit route,” <i>Journal of Experimental
    Medicine</i>, 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.” <i>Journal of Experimental
    Medicine</i>, vol. 215, no. 12, Rockefeller University Press, 2018, pp. 2959–61,
    doi:<a href="https://doi.org/10.1084/jem.20181934">10.1084/jem.20181934</a>.
  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: 2023-09-11T14:12:06Z
day: '20'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1084/jem.20181934
external_id:
  isi:
  - '000451920600002'
file:
- access_level: open_access
  checksum: 687beea1d64c213f4cb9e3c29ec11a14
  content_type: application/pdf
  creator: dernst
  date_created: 2019-02-06T08:49:52Z
  date_updated: 2020-07-14T12:47:09Z
  file_id: '5931'
  file_name: 2018_JournalExperMed_Reversat.pdf
  file_size: 1216437
  relation: main_file
file_date_updated: 2020-07-14T12:47:09Z
has_accepted_license: '1'
intvolume: '       215'
isi: 1
issue: '12'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-sa/4.0/
month: '11'
oa: 1
oa_version: Published Version
page: 2959-2961
publication: Journal of Experimental Medicine
publication_identifier:
  issn:
  - '00221007'
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
    BY-NC-SA 4.0)
  short: CC BY-NC-SA (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 215
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. <i>Journal
    of the Royal Society Interface</i>. 2018;15(149). doi:<a href="https://doi.org/10.1098/rsif.2018.0600">10.1098/rsif.2018.0600</a>
  apa: Hross, S., Theis, F. J., Sixt, M. K., &#38; Hasenauer, J. (2018). Mechanistic
    description of spatial processes using integrative modelling of noise-corrupted
    imaging data. <i>Journal of the Royal Society Interface</i>. Royal Society Publishing.
    <a href="https://doi.org/10.1098/rsif.2018.0600">https://doi.org/10.1098/rsif.2018.0600</a>
  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.” <i>Journal of the Royal Society Interface</i>. Royal Society Publishing,
    2018. <a href="https://doi.org/10.1098/rsif.2018.0600">https://doi.org/10.1098/rsif.2018.0600</a>.
  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,”
    <i>Journal of the Royal Society Interface</i>, 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.” <i>Journal of the Royal
    Society Interface</i>, vol. 15, no. 149, 20180600, Royal Society Publishing, 2018,
    doi:<a href="https://doi.org/10.1098/rsif.2018.0600">10.1098/rsif.2018.0600</a>.
  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: 2023-09-13T08:55:05Z
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:
  - '17425689'
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
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. <i>eLife</i>. 2018;7. doi:<a href="https://doi.org/10.7554/eLife.37888">10.7554/eLife.37888</a>
  apa: Alanko, J. H., &#38; Sixt, M. K. (2018). The cell sets the tone. <i>ELife</i>.
    eLife Sciences Publications. <a href="https://doi.org/10.7554/eLife.37888">https://doi.org/10.7554/eLife.37888</a>
  chicago: Alanko, Jonna H, and Michael K Sixt. “The Cell Sets the Tone.” <i>ELife</i>.
    eLife Sciences Publications, 2018. <a href="https://doi.org/10.7554/eLife.37888">https://doi.org/10.7554/eLife.37888</a>.
  ieee: J. H. Alanko and M. K. Sixt, “The cell sets the tone,” <i>eLife</i>, 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.” <i>ELife</i>,
    vol. 7, e37888, eLife Sciences Publications, 2018, doi:<a href="https://doi.org/10.7554/eLife.37888">10.7554/eLife.37888</a>.
  short: J.H. Alanko, M.K. Sixt, ELife 7 (2018).
date_created: 2019-01-20T22:59:19Z
date_published: 2018-06-06T00:00:00Z
date_updated: 2023-09-19T10:01:39Z
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:
  - 2050084X
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
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. <i>Nature Communications</i>. 2018;9(1).
    doi:<a href="https://doi.org/10.1038/s41467-018-04342-1">10.1038/s41467-018-04342-1</a>
  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. <i>Nature Communications</i>. Springer Nature.
    <a href="https://doi.org/10.1038/s41467-018-04342-1">https://doi.org/10.1038/s41467-018-04342-1</a>
  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.” <i>Nature Communications</i>. Springer Nature, 2018. <a href="https://doi.org/10.1038/s41467-018-04342-1">https://doi.org/10.1038/s41467-018-04342-1</a>.
  ieee: M. Morri <i>et al.</i>, “Optical functionalization of human class A orphan
    G-protein-coupled receptors,” <i>Nature Communications</i>, 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.” <i>Nature Communications</i>, vol. 9, no. 1, 1950,
    Springer Nature, 2018, doi:<a href="https://doi.org/10.1038/s41467-018-04342-1">10.1038/s41467-018-04342-1</a>.
  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: 2023-09-19T14:29:32Z
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. <i>Molecular
    Biology of the Cell</i>. 2018;29(22):2674-2686. doi:<a href="https://doi.org/10.1091/mbc.e18-02-0082">10.1091/mbc.e18-02-0082</a>
  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. <i>Molecular Biology of the
    Cell</i>. American Society for Cell Biology . <a href="https://doi.org/10.1091/mbc.e18-02-0082">https://doi.org/10.1091/mbc.e18-02-0082</a>
  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.” <i>Molecular Biology of the Cell</i>. American Society for Cell
    Biology , 2018. <a href="https://doi.org/10.1091/mbc.e18-02-0082">https://doi.org/10.1091/mbc.e18-02-0082</a>.
  ieee: S. Dolati <i>et al.</i>, “On the relation between filament density, force
    generation, and protrusion rate in mesenchymal cell motility,” <i>Molecular Biology
    of the Cell</i>, 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.” <i>Molecular Biology of the
    Cell</i>, vol. 29, no. 22, American Society for Cell Biology , 2018, pp. 2674–86,
    doi:<a href="https://doi.org/10.1091/mbc.e18-02-0082">10.1091/mbc.e18-02-0082</a>.
  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
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'
...
---
_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: ' FöFoLe project 947 (F.G.), the Friedrich-Baur-Stiftung project
  41/16 (F.G.)'
article_number: e3018
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. <i>Bio-Protocol</i>. 2018;8(18). doi:<a href="https://doi.org/10.21769/bioprotoc.3018">10.21769/bioprotoc.3018</a>
  apa: Fan, S., Lorenz, M., Massberg, S., &#38; Gärtner, F. R. (2018). Platelet migration
    and bacterial trapping assay under flow. <i>Bio-Protocol</i>. Bio-Protocol. <a
    href="https://doi.org/10.21769/bioprotoc.3018">https://doi.org/10.21769/bioprotoc.3018</a>
  chicago: Fan, Shuxia, Michael Lorenz, Steffen Massberg, and Florian R Gärtner. “Platelet
    Migration and Bacterial Trapping Assay under Flow.” <i>Bio-Protocol</i>. Bio-Protocol,
    2018. <a href="https://doi.org/10.21769/bioprotoc.3018">https://doi.org/10.21769/bioprotoc.3018</a>.
  ieee: S. Fan, M. Lorenz, S. Massberg, and F. R. Gärtner, “Platelet migration and
    bacterial trapping assay under flow,” <i>Bio-Protocol</i>, 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.” <i>Bio-Protocol</i>, vol. 8, no. 18, e3018, Bio-Protocol, 2018, doi:<a
    href="https://doi.org/10.21769/bioprotoc.3018">10.21769/bioprotoc.3018</a>.
  short: S. Fan, M. Lorenz, S. Massberg, F.R. Gärtner, Bio-Protocol 8 (2018).
date_created: 2019-04-29T09:40:33Z
date_published: 2018-09-20T00:00:00Z
date_updated: 2021-01-12T08:07:12Z
day: '20'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.21769/bioprotoc.3018
ec_funded: 1
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
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: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2018'
...
