[{"type":"journal_article","language":[{"iso":"eng"}],"publisher":"Cell Press","doi":"10.1016/j.it.2019.08.004","author":[{"first_name":"Leo","full_name":"Nicolai, Leo","last_name":"Nicolai"},{"id":"397A88EE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6120-3723","full_name":"Gärtner, Florian R","first_name":"Florian R","last_name":"Gärtner"},{"full_name":"Massberg, Steffen","first_name":"Steffen","last_name":"Massberg"}],"issue":"10","publication":"Trends in Immunology","date_published":"2019-10-01T00:00:00Z","external_id":{"pmid":["31601520"],"isi":["000493292100005"]},"oa_version":"None","isi":1,"volume":40,"project":[{"name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","grant_number":"747687","_id":"260AA4E2-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}],"date_updated":"2023-08-30T07:19:23Z","date_created":"2019-11-04T16:27:36Z","year":"2019","quality_controlled":"1","page":"922-938","pmid":1,"scopus_import":"1","publication_identifier":{"issn":["1471-4906"]},"article_processing_charge":"No","article_type":"review","publication_status":"published","title":"Platelets in host defense: Experimental and clinical insights","month":"10","_id":"6988","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","department":[{"_id":"MiSi"}],"abstract":[{"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.","lang":"eng"}],"status":"public","ec_funded":1,"intvolume":"        40","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>","short":"L. Nicolai, F.R. Gärtner, S. Massberg, Trends in Immunology 40 (2019) 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>.","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.","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>.","ista":"Nicolai L, Gärtner FR, Massberg S. 2019. Platelets in host defense: Experimental and clinical insights. Trends in Immunology. 40(10), 922–938.","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>"},"day":"01"},{"date_published":"2019-12-01T00:00:00Z","external_id":{"isi":["000497966900007"],"pmid":["31582855"]},"oa_version":"None","author":[{"last_name":"Yamada","first_name":"KM","full_name":"Yamada, KM"},{"orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt"}],"issue":"12","publication":"Nature Reviews Molecular Cell Biology","publisher":"Springer Nature","doi":"10.1038/s41580-019-0172-9","type":"journal_article","language":[{"iso":"eng"}],"article_processing_charge":"No","pmid":1,"scopus_import":"1","publication_identifier":{"issn":["1471-0072"],"eissn":["1471-0080"]},"date_updated":"2023-08-30T07:22:20Z","date_created":"2019-11-12T14:54:42Z","year":"2019","page":"738–752","quality_controlled":"1","isi":1,"volume":20,"department":[{"_id":"MiSi"}],"month":"12","_id":"7009","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","article_type":"review","publication_status":"published","title":"Mechanisms of 3D cell migration","day":"01","citation":{"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>.","ista":"Yamada K, Sixt MK. 2019. Mechanisms of 3D cell migration. Nature Reviews Molecular Cell Biology. 20(12), 738–752.","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.","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.","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>"},"intvolume":"        20","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."}],"status":"public"},{"department":[{"_id":"MiSi"}],"article_type":"original","title":"Persistent and polarized global actin flow is essential for directionality during cell migration","oa":1,"publication_status":"published","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","month":"11","_id":"7105","intvolume":"        21","citation":{"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>","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.","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.","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.","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>"},"day":"01","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."}],"status":"public","author":[{"full_name":"Yolland, Lawrence","first_name":"Lawrence","last_name":"Yolland"},{"last_name":"Burki","full_name":"Burki, Mubarik","first_name":"Mubarik"},{"first_name":"Stefania","full_name":"Marcotti, Stefania","last_name":"Marcotti"},{"first_name":"Andrei","full_name":"Luchici, Andrei","last_name":"Luchici"},{"last_name":"Kenny","first_name":"Fiona N.","full_name":"Kenny, Fiona N."},{"full_name":"Davis, John Robert","first_name":"John Robert","last_name":"Davis"},{"first_name":"Eduardo","full_name":"Serna-Morales, Eduardo","last_name":"Serna-Morales"},{"full_name":"Müller, Jan","first_name":"Jan","last_name":"Müller","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt"},{"full_name":"Davidson, Andrew","first_name":"Andrew","last_name":"Davidson"},{"last_name":"Wood","full_name":"Wood, Will","first_name":"Will"},{"full_name":"Schumacher, Linus J.","first_name":"Linus J.","last_name":"Schumacher"},{"first_name":"Robert G.","full_name":"Endres, Robert G.","last_name":"Endres"},{"last_name":"Miodownik","full_name":"Miodownik, Mark","first_name":"Mark"},{"last_name":"Stramer","first_name":"Brian M.","full_name":"Stramer, Brian M."}],"publication":"Nature Cell Biology","issue":"11","date_published":"2019-11-01T00:00:00Z","oa_version":"Submitted Version","external_id":{"pmid":["31685997"],"isi":["000495888300009"]},"type":"journal_article","language":[{"iso":"eng"}],"publisher":"Springer Nature","doi":"10.1038/s41556-019-0411-5","scopus_import":"1","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7025891","open_access":"1"}],"pmid":1,"publication_identifier":{"eissn":["1476-4679"],"issn":["1465-7392"]},"article_processing_charge":"No","volume":21,"isi":1,"date_updated":"2023-09-06T11:08:52Z","quality_controlled":"1","page":"1370-1381","date_created":"2019-11-25T08:55:00Z","year":"2019"},{"abstract":[{"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.","lang":"eng"}],"status":"public","article_number":"dev171397","day":"04","citation":{"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>.","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.","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>.","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.","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>","short":"T. Stürner, A. Tatarnikova, J. Müller, B. Schaffran, H. Cuntz, Y. Zhang, M. Nemethova, S. Bogdan, V. Small, G. Tavosanis, Development 146 (2019)."},"intvolume":"       146","_id":"7404","month":"04","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","article_type":"original","publication_status":"published","title":"Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo","oa":1,"department":[{"_id":"MiSi"}],"date_updated":"2023-09-07T14:47:00Z","date_created":"2020-01-29T16:27:10Z","year":"2019","quality_controlled":"1","isi":1,"volume":146,"article_processing_charge":"No","pmid":1,"main_file_link":[{"url":"https://doi.org/10.1242/dev.171397","open_access":"1"}],"scopus_import":"1","publication_identifier":{"issn":["0950-1991"],"eissn":["1477-9129"]},"publisher":"The Company of Biologists","doi":"10.1242/dev.171397","type":"journal_article","language":[{"iso":"eng"}],"date_published":"2019-04-04T00:00:00Z","oa_version":"Published Version","external_id":{"pmid":["30910826"],"isi":["000464583200006"]},"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","last_name":"Müller","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D"},{"full_name":"Schaffran, Barbara","first_name":"Barbara","last_name":"Schaffran"},{"first_name":"Hermann","full_name":"Cuntz, Hermann","last_name":"Cuntz"},{"full_name":"Zhang, Yun","first_name":"Yun","last_name":"Zhang"},{"id":"34E27F1C-F248-11E8-B48F-1D18A9856A87","last_name":"Nemethova","first_name":"Maria","full_name":"Nemethova, Maria"},{"last_name":"Bogdan","first_name":"Sven","full_name":"Bogdan, Sven"},{"last_name":"Small","first_name":"Vic","full_name":"Small, Vic"},{"first_name":"Gaia","full_name":"Tavosanis, Gaia","last_name":"Tavosanis"}],"publication":"Development","issue":"7"},{"citation":{"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>.","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>.","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.","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).","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>"},"intvolume":"       132","day":"07","abstract":[{"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.","lang":"eng"}],"article_number":"jcs233387","status":"public","department":[{"_id":"MiSi"}],"article_type":"original","oa":1,"title":"GGA2 and RAB13 promote activity-dependent β1-integrin recycling","publication_status":"published","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","month":"06","_id":"7420","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1242/jcs.233387"}],"pmid":1,"publication_identifier":{"issn":["0021-9533"],"eissn":["1477-9137"]},"article_processing_charge":"No","volume":132,"isi":1,"date_updated":"2023-09-06T15:01:00Z","quality_controlled":"1","year":"2019","date_created":"2020-01-30T10:31:42Z","author":[{"last_name":"Sahgal","first_name":"Pranshu","full_name":"Sahgal, Pranshu"},{"first_name":"Jonna H","full_name":"Alanko, Jonna H","last_name":"Alanko","orcid":"0000-0002-7698-3061","id":"2CC12E8C-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Icha, Jaroslav","first_name":"Jaroslav","last_name":"Icha"},{"last_name":"Paatero","first_name":"Ilkka","full_name":"Paatero, Ilkka"},{"first_name":"Hellyeh","full_name":"Hamidi, Hellyeh","last_name":"Hamidi"},{"full_name":"Arjonen, Antti","first_name":"Antti","last_name":"Arjonen"},{"last_name":"Pietilä","full_name":"Pietilä, Mika","first_name":"Mika"},{"first_name":"Anne","full_name":"Rokka, Anne","last_name":"Rokka"},{"last_name":"Ivaska","full_name":"Ivaska, Johanna","first_name":"Johanna"}],"issue":"11","publication":"Journal of Cell Science","date_published":"2019-06-07T00:00:00Z","external_id":{"pmid":["31076515"],"isi":["000473327900017"]},"oa_version":"Published Version","type":"journal_article","language":[{"iso":"eng"}],"publisher":"The Company of Biologists","doi":"10.1242/jcs.233387"},{"citation":{"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.","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>.","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>","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>.","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.","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.","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>"},"intvolume":"       568","day":"25","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."}],"status":"public","ec_funded":1,"department":[{"_id":"MiSi"},{"_id":"NanoFab"},{"_id":"Bio"}],"article_type":"letter_note","title":"Nuclear positioning facilitates amoeboid migration along the path of least resistance","related_material":{"link":[{"relation":"press_release","description":"News on IST Homepage","url":"https://ist.ac.at/en/news/leukocytes-use-their-nucleus-as-a-ruler-to-choose-path-of-least-resistance/"}],"record":[{"status":"public","relation":"dissertation_contains","id":"14697"},{"relation":"dissertation_contains","status":"public","id":"6891"}]},"oa":1,"publication_status":"published","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","_id":"6328","month":"04","scopus_import":"1","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217284/","open_access":"1"}],"pmid":1,"article_processing_charge":"No","volume":568,"isi":1,"date_updated":"2024-03-25T23:30:22Z","project":[{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556"},{"name":"Cellular navigation along spatial gradients","grant_number":"724373","_id":"25FE9508-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"name":"Nano-Analytics of Cellular Systems","grant_number":"W01250-B20","_id":"265FAEBA-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"call_identifier":"FP7","grant_number":"291734","name":"International IST Postdoc Fellowship Programme","_id":"25681D80-B435-11E9-9278-68D0E5697425"},{"grant_number":"ALTF 1396-2014","name":"Molecular and system level view of immune cell migration","_id":"25A48D24-B435-11E9-9278-68D0E5697425"}],"acknowledged_ssus":[{"_id":"SSU"}],"page":"546-550","quality_controlled":"1","year":"2019","date_created":"2019-04-17T06:52:28Z","author":[{"last_name":"Renkawitz","full_name":"Renkawitz, Jörg","first_name":"Jörg","orcid":"0000-0003-2856-3369","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Kopf","first_name":"Aglaja","full_name":"Kopf, Aglaja","id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-2187-6656"},{"id":"489E3F00-F248-11E8-B48F-1D18A9856A87","last_name":"Stopp","full_name":"Stopp, Julian A","first_name":"Julian A"},{"first_name":"Ingrid","full_name":"de Vries, Ingrid","last_name":"de Vries","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Driscoll","full_name":"Driscoll, Meghan K.","first_name":"Meghan K."},{"full_name":"Merrin, Jack","first_name":"Jack","last_name":"Merrin","id":"4515C308-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5145-4609"},{"orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert","full_name":"Hauschild, Robert","last_name":"Hauschild"},{"full_name":"Welf, Erik S.","first_name":"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"},{"last_name":"Sixt","first_name":"Michael K","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"publication":"Nature","date_published":"2019-04-25T00:00:00Z","oa_version":"Submitted Version","external_id":{"pmid":["30944468"],"isi":["000465594200050"]},"type":"journal_article","language":[{"iso":"eng"}],"publisher":"Springer Nature","doi":"10.1038/s41586-019-1087-5"},{"ec_funded":1,"abstract":[{"lang":"eng","text":"Platelets are small anucleate cellular fragments that are released by megakaryocytes and safeguard vascular integrity through a process termed ‘haemostasis’. However, platelets have important roles beyond haemostasis as they contribute to the initiation and coordination of intravascular immune responses. They continuously monitor blood vessel integrity and tightly coordinate vascular trafficking and functions of multiple cell types. In this way platelets act as ‘patrolling officers of the vascular highway’ that help to establish effective immune responses to infections and cancer. Here we discuss the distinct biological features of platelets that allow them to shape immune responses to pathogens and tumour cells, highlighting the parallels between these responses."}],"status":"public","day":"01","intvolume":"        19","citation":{"ista":"Gärtner FR, Massberg S. 2019. Patrolling the vascular borders: Platelets in immunity to infection and cancer. Nature Reviews Immunology. 19(12), 747–760.","chicago":"Gärtner, Florian R, and Steffen Massberg. “Patrolling the Vascular Borders: Platelets in Immunity to Infection and Cancer.” <i>Nature Reviews Immunology</i>. Springer Nature, 2019. <a href=\"https://doi.org/10.1038/s41577-019-0202-z\">https://doi.org/10.1038/s41577-019-0202-z</a>.","apa":"Gärtner, F. R., &#38; Massberg, S. (2019). Patrolling the vascular borders: Platelets in immunity to infection and cancer. <i>Nature Reviews Immunology</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41577-019-0202-z\">https://doi.org/10.1038/s41577-019-0202-z</a>","mla":"Gärtner, Florian R., and Steffen Massberg. “Patrolling the Vascular Borders: Platelets in Immunity to Infection and Cancer.” <i>Nature Reviews Immunology</i>, vol. 19, no. 12, Springer Nature, 2019, pp. 747–760, doi:<a href=\"https://doi.org/10.1038/s41577-019-0202-z\">10.1038/s41577-019-0202-z</a>.","ieee":"F. R. Gärtner and S. Massberg, “Patrolling the vascular borders: Platelets in immunity to infection and cancer,” <i>Nature Reviews Immunology</i>, vol. 19, no. 12. Springer Nature, pp. 747–760, 2019.","short":"F.R. Gärtner, S. Massberg, Nature Reviews Immunology 19 (2019) 747–760.","ama":"Gärtner FR, Massberg S. Patrolling the vascular borders: Platelets in immunity to infection and cancer. <i>Nature Reviews Immunology</i>. 2019;19(12):747–760. doi:<a href=\"https://doi.org/10.1038/s41577-019-0202-z\">10.1038/s41577-019-0202-z</a>"},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","month":"12","_id":"6824","article_type":"original","title":"Patrolling the vascular borders: Platelets in immunity to infection and cancer","publication_status":"published","department":[{"_id":"MiSi"}],"date_updated":"2023-08-29T07:16:14Z","project":[{"call_identifier":"H2020","name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","grant_number":"747687","_id":"260AA4E2-B435-11E9-9278-68D0E5697425"}],"quality_controlled":"1","page":"747–760","date_created":"2019-08-20T17:24:32Z","year":"2019","volume":19,"isi":1,"article_processing_charge":"No","scopus_import":"1","pmid":1,"publication_identifier":{"eissn":["1474-1741"],"issn":["1474-1733"]},"publisher":"Springer Nature","doi":"10.1038/s41577-019-0202-z","type":"journal_article","language":[{"iso":"eng"}],"date_published":"2019-12-01T00:00:00Z","oa_version":"None","external_id":{"pmid":["31409920"],"isi":["000499090600011"]},"author":[{"id":"397A88EE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6120-3723","last_name":"Gärtner","first_name":"Florian R","full_name":"Gärtner, Florian R"},{"last_name":"Massberg","first_name":"Steffen","full_name":"Massberg, Steffen"}],"issue":"12","publication":"Nature Reviews Immunology"},{"article_processing_charge":"No","publication_identifier":{"issn":["0092-8674"],"eissn":["1097-4172"]},"pmid":1,"scopus_import":"1","date_created":"2019-09-15T22:00:46Z","year":"2019","page":"51-53","quality_controlled":"1","date_updated":"2024-03-25T23:30:22Z","isi":1,"volume":179,"oa_version":"None","external_id":{"isi":["000486618500011"],"pmid":["31539498"]},"date_published":"2019-09-19T00:00:00Z","publication":"Cell","issue":"1","author":[{"id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-2187-6656","last_name":"Kopf","first_name":"Aglaja","full_name":"Kopf, Aglaja"},{"last_name":"Sixt","first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"doi":"10.1016/j.cell.2019.08.047","publisher":"Elsevier","language":[{"iso":"eng"}],"type":"journal_article","day":"19","intvolume":"       179","citation":{"short":"A. Kopf, M.K. Sixt, Cell 179 (2019) 51–53.","ama":"Kopf A, Sixt MK. The neural crest pitches in to remove apoptotic debris. <i>Cell</i>. 2019;179(1):51-53. doi:<a href=\"https://doi.org/10.1016/j.cell.2019.08.047\">10.1016/j.cell.2019.08.047</a>","ista":"Kopf A, Sixt MK. 2019. The neural crest pitches in to remove apoptotic debris. Cell. 179(1), 51–53.","apa":"Kopf, A., &#38; Sixt, M. K. (2019). The neural crest pitches in to remove apoptotic debris. <i>Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cell.2019.08.047\">https://doi.org/10.1016/j.cell.2019.08.047</a>","chicago":"Kopf, Aglaja, and Michael K Sixt. “The Neural Crest Pitches in to Remove Apoptotic Debris.” <i>Cell</i>. Elsevier, 2019. <a href=\"https://doi.org/10.1016/j.cell.2019.08.047\">https://doi.org/10.1016/j.cell.2019.08.047</a>.","ieee":"A. Kopf and M. K. Sixt, “The neural crest pitches in to remove apoptotic debris,” <i>Cell</i>, vol. 179, no. 1. Elsevier, pp. 51–53, 2019.","mla":"Kopf, Aglaja, and Michael K. Sixt. “The Neural Crest Pitches in to Remove Apoptotic Debris.” <i>Cell</i>, vol. 179, no. 1, Elsevier, 2019, pp. 51–53, doi:<a href=\"https://doi.org/10.1016/j.cell.2019.08.047\">10.1016/j.cell.2019.08.047</a>."},"status":"public","department":[{"_id":"MiSi"}],"_id":"6877","month":"09","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_status":"published","related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"6891"}]},"title":"The neural crest pitches in to remove apoptotic debris","article_type":"original"},{"publication_status":"published","related_material":{"record":[{"status":"public","relation":"part_of_dissertation","id":"6328"},{"status":"public","relation":"part_of_dissertation","id":"15"},{"id":"6877","status":"public","relation":"part_of_dissertation"}],"link":[{"relation":"press_release","url":"https://ist.ac.at/en/news/feeling-like-a-cell/"}]},"oa":1,"title":"The implication of cytoskeletal dynamics on leukocyte migration","month":"07","_id":"6891","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","alternative_title":["ISTA Thesis"],"department":[{"_id":"MiSi"}],"abstract":[{"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","lang":"eng"}],"status":"public","degree_awarded":"PhD","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>","short":"A. Kopf, The Implication of Cytoskeletal Dynamics on Leukocyte Migration, Institute of Science and Technology Austria, 2019.","ieee":"A. Kopf, “The implication of cytoskeletal dynamics on leukocyte migration,” Institute of Science and Technology Austria, 2019.","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>.","ista":"Kopf A. 2019. The implication of cytoskeletal dynamics on leukocyte migration. Institute of Science and Technology Austria.","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>.","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>"},"keyword":["cell biology","immunology","leukocyte","migration","microfluidics"],"supervisor":[{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"has_accepted_license":"1","day":"24","type":"dissertation","file_date_updated":"2020-10-17T22:30:03Z","language":[{"iso":"eng"}],"publisher":"Institute of Science and Technology Austria","doi":"10.15479/AT:ISTA:6891","author":[{"orcid":"0000-0002-2187-6656","id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87","last_name":"Kopf","first_name":"Aglaja","full_name":"Kopf, Aglaja"}],"ddc":["570"],"date_published":"2019-07-24T00:00:00Z","oa_version":"Published Version","file":[{"relation":"source_file","checksum":"00d100d6468e31e583051e0a006b640c","file_size":74735267,"creator":"akopf","file_name":"Kopf_PhD_Thesis.docx","embargo_to":"open_access","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","date_created":"2019-10-15T05:28:42Z","file_id":"6950","access_level":"closed","date_updated":"2020-10-17T22:30:03Z"},{"creator":"akopf","file_size":52787224,"checksum":"5d1baa899993ae6ca81aebebe1797000","relation":"main_file","access_level":"open_access","date_updated":"2020-10-17T22:30:03Z","file_id":"6951","content_type":"application/pdf","date_created":"2019-10-15T05:28:47Z","embargo":"2020-10-16","file_name":"Kopf_PhD_Thesis1.pdf"}],"project":[{"_id":"265E2996-B435-11E9-9278-68D0E5697425","grant_number":"W01250-B20","name":"Nano-Analytics of Cellular Systems","call_identifier":"FWF"}],"date_updated":"2023-10-18T08:49:17Z","year":"2019","date_created":"2019-09-19T08:19:44Z","page":"171","publication_identifier":{"isbn":["978-3-99078-002-2"],"eissn":["2663-337X"]},"article_processing_charge":"No"},{"scopus_import":"1","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pubmed/29777221"}],"pmid":1,"article_processing_charge":"No","volume":19,"isi":1,"page":"606 - 616","quality_controlled":"1","date_created":"2018-12-11T11:44:10Z","year":"2018","date_updated":"2024-03-25T23:30:22Z","acknowledged_ssus":[{"_id":"SSU"}],"project":[{"call_identifier":"H2020","_id":"25FE9508-B435-11E9-9278-68D0E5697425","name":"Cellular navigation along spatial gradients","grant_number":"724373"},{"call_identifier":"H2020","name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","grant_number":"747687","_id":"260AA4E2-B435-11E9-9278-68D0E5697425"},{"_id":"25A48D24-B435-11E9-9278-68D0E5697425","name":"Molecular and system level view of immune cell migration","grant_number":"ALTF 1396-2014"},{"_id":"25A603A2-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556","call_identifier":"FP7"}],"publication":"Nature Immunology","publist_id":"8040","issue":"6","author":[{"orcid":"0000-0002-6625-3348","id":"4167FE56-F248-11E8-B48F-1D18A9856A87","full_name":"Hons, Miroslav","first_name":"Miroslav","last_name":"Hons"},{"orcid":"0000-0002-2187-6656","id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87","last_name":"Kopf","full_name":"Kopf, Aglaja","first_name":"Aglaja"},{"orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert","full_name":"Hauschild, Robert","last_name":"Hauschild"},{"id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1073-744X","last_name":"Leithner","full_name":"Leithner, Alexander F","first_name":"Alexander F"},{"orcid":"0000-0001-6120-3723","id":"397A88EE-F248-11E8-B48F-1D18A9856A87","first_name":"Florian R","full_name":"Gärtner, Florian R","last_name":"Gärtner"},{"last_name":"Abe","first_name":"Jun","full_name":"Abe, Jun"},{"id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2856-3369","last_name":"Renkawitz","full_name":"Renkawitz, Jörg","first_name":"Jörg"},{"last_name":"Stein","first_name":"Jens","full_name":"Stein, Jens"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt"}],"external_id":{"pmid":["29777221"],"isi":["000433041500026"]},"oa_version":"Published Version","date_published":"2018-05-18T00:00:00Z","language":[{"iso":"eng"}],"type":"journal_article","doi":"10.1038/s41590-018-0109-z","publisher":"Nature Publishing Group","citation":{"short":"M. Hons, A. Kopf, R. Hauschild, A.F. Leithner, F.R. Gärtner, J. Abe, J. Renkawitz, J. Stein, M.K. Sixt, Nature Immunology 19 (2018) 606–616.","ama":"Hons M, Kopf A, Hauschild R, et al. Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. <i>Nature Immunology</i>. 2018;19(6):606-616. doi:<a href=\"https://doi.org/10.1038/s41590-018-0109-z\">10.1038/s41590-018-0109-z</a>","apa":"Hons, M., Kopf, A., Hauschild, R., Leithner, A. F., Gärtner, F. R., Abe, J., … Sixt, M. K. (2018). Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. <i>Nature Immunology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/s41590-018-0109-z\">https://doi.org/10.1038/s41590-018-0109-z</a>","ista":"Hons M, Kopf A, Hauschild R, Leithner AF, Gärtner FR, Abe J, Renkawitz J, Stein J, Sixt MK. 2018. Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. 19(6), 606–616.","chicago":"Hons, Miroslav, Aglaja Kopf, Robert Hauschild, Alexander F Leithner, Florian R Gärtner, Jun Abe, Jörg Renkawitz, Jens Stein, and Michael K Sixt. “Chemokines and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal Migration of T Cells.” <i>Nature Immunology</i>. Nature Publishing Group, 2018. <a href=\"https://doi.org/10.1038/s41590-018-0109-z\">https://doi.org/10.1038/s41590-018-0109-z</a>.","mla":"Hons, Miroslav, et al. “Chemokines and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal Migration of T Cells.” <i>Nature Immunology</i>, vol. 19, no. 6, Nature Publishing Group, 2018, pp. 606–16, doi:<a href=\"https://doi.org/10.1038/s41590-018-0109-z\">10.1038/s41590-018-0109-z</a>.","ieee":"M. Hons <i>et al.</i>, “Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells,” <i>Nature Immunology</i>, vol. 19, no. 6. Nature Publishing Group, pp. 606–616, 2018."},"intvolume":"        19","day":"18","status":"public","abstract":[{"text":"Although much is known about the physiological framework of T cell motility, and numerous rate-limiting molecules have been identified through loss-of-function approaches, an integrated functional concept of T cell motility is lacking. Here, we used in vivo precision morphometry together with analysis of cytoskeletal dynamics in vitro to deconstruct the basic mechanisms of T cell migration within lymphatic organs. We show that the contributions of the integrin LFA-1 and the chemokine receptor CCR7 are complementary rather than positioned in a linear pathway, as they are during leukocyte extravasation from the blood vasculature. Our data demonstrate that CCR7 controls cortical actin flows, whereas integrins mediate substrate friction that is sufficient to drive locomotion in the absence of considerable surface adhesions and plasma membrane flux.","lang":"eng"}],"ec_funded":1,"department":[{"_id":"MiSi"},{"_id":"Bio"}],"acknowledgement":"This work was funded by grants from the European Research Council (ERC StG 281556 and CoG 724373) and the Austrian Science Foundation (FWF) to M.S. and by Swiss National Foundation (SNF) project grants 31003A_135649, 31003A_153457 and CR23I3_156234 to J.V.S. F.G. received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 747687, and J.R. was funded by an EMBO long-term fellowship (ALTF 1396-2014).","related_material":{"record":[{"id":"6891","status":"public","relation":"dissertation_contains"}]},"oa":1,"title":"Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells","publication_status":"published","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","month":"05","_id":"15"},{"type":"book_chapter","language":[{"iso":"eng"}],"publisher":"Academic Press","doi":"10.1016/bs.mcb.2018.07.004","author":[{"orcid":"0000-0003-2856-3369","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","last_name":"Renkawitz","full_name":"Renkawitz, Jörg","first_name":"Jörg"},{"last_name":"Reversat","full_name":"Reversat, Anne","first_name":"Anne","id":"35B76592-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-0666-8928"},{"id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1073-744X","full_name":"Leithner, Alexander F","first_name":"Alexander F","last_name":"Leithner"},{"full_name":"Merrin, Jack","first_name":"Jack","last_name":"Merrin","id":"4515C308-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5145-4609"},{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"publication":"Methods in Cell Biology","publist_id":"7768","date_published":"2018-07-27T00:00:00Z","external_id":{"pmid":["30165964"],"isi":["000452412300006"]},"oa_version":"None","isi":1,"volume":147,"date_updated":"2023-09-13T08:56:35Z","date_created":"2018-12-11T11:44:54Z","year":"2018","quality_controlled":"1","page":"79 - 91","pmid":1,"scopus_import":"1","publication_identifier":{"issn":["0091679X"]},"article_processing_charge":"No","publication_status":"published","title":"Micro-engineered “pillar forests” to study cell migration in complex but controlled 3D environments","month":"07","_id":"153","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","department":[{"_id":"MiSi"},{"_id":"NanoFab"}],"abstract":[{"text":"Cells migrating in multicellular organisms steadily traverse complex three-dimensional (3D) environments. To decipher the underlying cell biology, current experimental setups either use simplified 2D, tissue-mimetic 3D (e.g., collagen matrices) or in vivo environments. While only in vivo experiments are truly physiological, they do not allow for precise manipulation of environmental parameters. 2D in vitro experiments do allow mechanical and chemical manipulations, but increasing evidence demonstrates substantial differences of migratory mechanisms in 2D and 3D. Here, we describe simple, robust, and versatile “pillar forests” to investigate cell migration in complex but fully controllable 3D environments. Pillar forests are polydimethylsiloxane-based setups, in which two closely adjacent surfaces are interconnected by arrays of micrometer-sized pillars. Changing the pillar shape, size, height and the inter-pillar distance precisely manipulates microenvironmental parameters (e.g., pore sizes, micro-geometry, micro-topology), while being easily combined with chemotactic cues, surface coatings, diverse cell types and advanced imaging techniques. Thus, pillar forests combine the advantages of 2D cell migration assays with the precise definition of 3D environmental parameters.","lang":"eng"}],"status":"public","citation":{"ista":"Renkawitz J, Reversat A, Leithner AF, Merrin J, Sixt MK. 2018.Micro-engineered “pillar forests” to study cell migration in complex but controlled 3D environments. In: Methods in Cell Biology. vol. 147, 79–91.","apa":"Renkawitz, J., Reversat, A., Leithner, A. F., Merrin, J., &#38; Sixt, M. K. (2018). Micro-engineered “pillar forests” to study cell migration in complex but controlled 3D environments. In <i>Methods in Cell Biology</i> (Vol. 147, pp. 79–91). Academic Press. <a href=\"https://doi.org/10.1016/bs.mcb.2018.07.004\">https://doi.org/10.1016/bs.mcb.2018.07.004</a>","chicago":"Renkawitz, Jörg, Anne Reversat, Alexander F Leithner, Jack Merrin, and Michael K Sixt. “Micro-Engineered ‘Pillar Forests’ to Study Cell Migration in Complex but Controlled 3D Environments.” In <i>Methods in Cell Biology</i>, 147:79–91. Academic Press, 2018. <a href=\"https://doi.org/10.1016/bs.mcb.2018.07.004\">https://doi.org/10.1016/bs.mcb.2018.07.004</a>.","ieee":"J. Renkawitz, A. Reversat, A. F. Leithner, J. Merrin, and M. K. Sixt, “Micro-engineered ‘pillar forests’ to study cell migration in complex but controlled 3D environments,” in <i>Methods in Cell Biology</i>, vol. 147, Academic Press, 2018, pp. 79–91.","mla":"Renkawitz, Jörg, et al. “Micro-Engineered ‘Pillar Forests’ to Study Cell Migration in Complex but Controlled 3D Environments.” <i>Methods in Cell Biology</i>, vol. 147, Academic Press, 2018, pp. 79–91, doi:<a href=\"https://doi.org/10.1016/bs.mcb.2018.07.004\">10.1016/bs.mcb.2018.07.004</a>.","short":"J. Renkawitz, A. Reversat, A.F. Leithner, J. Merrin, M.K. Sixt, in:, Methods in Cell Biology, Academic Press, 2018, pp. 79–91.","ama":"Renkawitz J, Reversat A, Leithner AF, Merrin J, Sixt MK. Micro-engineered “pillar forests” to study cell migration in complex but controlled 3D environments. In: <i>Methods in Cell Biology</i>. Vol 147. Academic Press; 2018:79-91. doi:<a href=\"https://doi.org/10.1016/bs.mcb.2018.07.004\">10.1016/bs.mcb.2018.07.004</a>"},"intvolume":"       147","day":"27"},{"publisher":"Rockefeller University Press","doi":"10.1084/jem.20181934","file_date_updated":"2020-07-14T12:47:09Z","type":"journal_article","language":[{"iso":"eng"}],"date_published":"2018-11-20T00:00:00Z","external_id":{"isi":["000451920600002"]},"oa_version":"Published Version","ddc":["570"],"author":[{"id":"35B76592-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-0666-8928","first_name":"Anne","full_name":"Reversat, Anne","last_name":"Reversat"},{"last_name":"Sixt","first_name":"Michael K","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"issue":"12","publication":"Journal of Experimental Medicine","date_updated":"2023-09-11T14:12:06Z","quality_controlled":"1","page":"2959-2961","date_created":"2018-12-16T22:59:18Z","year":"2018","volume":215,"isi":1,"file":[{"content_type":"application/pdf","date_created":"2019-02-06T08:49:52Z","file_id":"5931","access_level":"open_access","date_updated":"2020-07-14T12:47:09Z","file_name":"2018_JournalExperMed_Reversat.pdf","file_size":1216437,"creator":"dernst","relation":"main_file","checksum":"687beea1d64c213f4cb9e3c29ec11a14"}],"article_processing_charge":"No","tmp":{"short":"CC BY-NC-SA (4.0)","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)"},"scopus_import":"1","publication_identifier":{"issn":["00221007"]},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","_id":"5672","month":"11","title":"IgM's exit route","oa":1,"publication_status":"published","department":[{"_id":"MiSi"}],"abstract":[{"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.","lang":"eng"}],"status":"public","has_accepted_license":"1","day":"20","citation":{"short":"A. Reversat, M.K. Sixt, Journal of Experimental Medicine 215 (2018) 2959–2961.","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>","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>.","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>","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>.","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."},"intvolume":"       215"},{"intvolume":"        15","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>","short":"S. Hross, F.J. Theis, M.K. Sixt, J. Hasenauer, Journal of the Royal Society Interface 15 (2018).","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.","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>.","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>.","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."},"has_accepted_license":"1","day":"05","abstract":[{"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.","lang":"eng"}],"status":"public","article_number":"20180600","department":[{"_id":"MiSi"}],"publication_status":"published","title":"Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data","oa":1,"_id":"5858","month":"12","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","scopus_import":"1","publication_identifier":{"issn":["17425689"]},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"article_processing_charge":"No","file":[{"file_name":"2018_Interface_Hross.pdf","file_id":"5925","content_type":"application/pdf","date_created":"2019-02-05T14:46:44Z","date_updated":"2020-07-14T12:47:13Z","access_level":"open_access","relation":"main_file","checksum":"56eb4308a15b7190bff938fab1f780e8","file_size":1464288,"creator":"dernst"}],"isi":1,"volume":15,"date_updated":"2023-09-13T08:55:05Z","year":"2018","date_created":"2019-01-20T22:59:18Z","quality_controlled":"1","author":[{"full_name":"Hross, Sabrina","first_name":"Sabrina","last_name":"Hross"},{"last_name":"Theis","first_name":"Fabian J.","full_name":"Theis, Fabian J."},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","first_name":"Michael K","full_name":"Sixt, Michael K","last_name":"Sixt"},{"first_name":"Jan","full_name":"Hasenauer, Jan","last_name":"Hasenauer"}],"ddc":["570"],"publication":"Journal of the Royal Society Interface","issue":"149","date_published":"2018-12-05T00:00:00Z","external_id":{"isi":["000456783800011"]},"oa_version":"Published Version","type":"journal_article","file_date_updated":"2020-07-14T12:47:13Z","language":[{"iso":"eng"}],"publisher":"Royal Society Publishing","doi":"10.1098/rsif.2018.0600"},{"month":"06","_id":"5861","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publication_status":"published","oa":1,"title":"The cell sets the tone","article_type":"original","department":[{"_id":"MiSi"}],"status":"public","article_number":"e37888","abstract":[{"text":"In zebrafish larvae, it is the cell type that determines how the cell responds to a chemokine signal.","lang":"eng"}],"day":"06","has_accepted_license":"1","citation":{"ista":"Alanko JH, Sixt MK. 2018. The cell sets the tone. eLife. 7, e37888.","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>.","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>","ieee":"J. H. Alanko and M. K. Sixt, “The cell sets the tone,” <i>eLife</i>, vol. 7. eLife Sciences Publications, 2018.","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).","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>"},"intvolume":"         7","doi":"10.7554/eLife.37888","publisher":"eLife Sciences Publications","language":[{"iso":"eng"}],"type":"journal_article","file_date_updated":"2020-07-14T12:47:13Z","external_id":{"isi":["000434375000001"]},"oa_version":"Published Version","date_published":"2018-06-06T00:00:00Z","publication":"eLife","author":[{"first_name":"Jonna H","full_name":"Alanko, Jonna H","last_name":"Alanko","orcid":"0000-0002-7698-3061","id":"2CC12E8C-F248-11E8-B48F-1D18A9856A87"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","first_name":"Michael K","full_name":"Sixt, Michael K","last_name":"Sixt"}],"ddc":["570"],"year":"2018","date_created":"2019-01-20T22:59:19Z","quality_controlled":"1","date_updated":"2023-09-19T10:01:39Z","file":[{"file_id":"5973","content_type":"application/pdf","date_created":"2019-02-13T10:52:11Z","date_updated":"2020-07-14T12:47:13Z","access_level":"open_access","file_name":"2018_eLife_Alanko.pdf","file_size":358141,"creator":"dernst","relation":"main_file","checksum":"f1c7ec2a809408d763c4b529a98f9a3b"}],"isi":1,"volume":7,"article_processing_charge":"No","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"publication_identifier":{"issn":["2050084X"]},"scopus_import":"1"},{"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","status":"public","ec_funded":1,"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>","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).","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>.","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.","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>.","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."},"intvolume":"         9","has_accepted_license":"1","day":"01","title":"Optical functionalization of human class A orphan G-protein-coupled receptors","oa":1,"publication_status":"published","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","month":"12","_id":"5984","department":[{"_id":"HaJa"},{"_id":"CaGu"},{"_id":"MiSi"}],"volume":9,"isi":1,"file":[{"relation":"main_file","checksum":"8325fcc194264af4749e662a73bf66b5","file_size":1349914,"creator":"kschuh","file_name":"2018_Springer_Morri.pdf","file_id":"5985","content_type":"application/pdf","date_created":"2019-02-14T10:58:29Z","access_level":"open_access","date_updated":"2020-07-14T12:47:14Z"}],"date_updated":"2023-09-19T14:29:32Z","project":[{"call_identifier":"FP7","name":"Microbial Ion Channels for Synthetic Neurobiology","grant_number":"303564","_id":"25548C20-B435-11E9-9278-68D0E5697425"},{"call_identifier":"FWF","_id":"255A6082-B435-11E9-9278-68D0E5697425","name":"Molecular Drug Targets","grant_number":"W1232-B24"}],"quality_controlled":"1","year":"2018","date_created":"2019-02-14T10:50:24Z","scopus_import":"1","publication_identifier":{"issn":["2041-1723"]},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"article_processing_charge":"No","file_date_updated":"2020-07-14T12:47:14Z","type":"journal_article","language":[{"iso":"eng"}],"publisher":"Springer Nature","doi":"10.1038/s41467-018-04342-1","ddc":["570"],"author":[{"id":"4863116E-F248-11E8-B48F-1D18A9856A87","last_name":"Morri","full_name":"Morri, Maurizio","first_name":"Maurizio"},{"last_name":"Sanchez-Romero","first_name":"Inmaculada","full_name":"Sanchez-Romero, Inmaculada","id":"3D9C5D30-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Tichy","first_name":"Alexandra-Madelaine","full_name":"Tichy, Alexandra-Madelaine","id":"29D8BB2C-F248-11E8-B48F-1D18A9856A87"},{"id":"32CFBA64-F248-11E8-B48F-1D18A9856A87","last_name":"Kainrath","full_name":"Kainrath, Stephanie","first_name":"Stephanie"},{"full_name":"Gerrard, Elliot J.","first_name":"Elliot J.","last_name":"Gerrard"},{"first_name":"Priscila","full_name":"Hirschfeld, Priscila","last_name":"Hirschfeld","id":"435ACB3A-F248-11E8-B48F-1D18A9856A87"},{"id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","first_name":"Jan","full_name":"Schwarz, Jan","last_name":"Schwarz"},{"id":"33BA6C30-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-8023-9315","first_name":"Harald L","full_name":"Janovjak, Harald L","last_name":"Janovjak"}],"publication":"Nature Communications","issue":"1","date_published":"2018-12-01T00:00:00Z","external_id":{"isi":["000432280000006"]},"oa_version":"Published Version"},{"status":"public","abstract":[{"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.","lang":"eng"}],"day":"01","has_accepted_license":"1","intvolume":"        29","citation":{"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.","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>.","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>.","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.","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>","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>","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."},"month":"11","_id":"5992","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publication_status":"published","title":"On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility","oa":1,"department":[{"_id":"MiSi"}],"year":"2018","date_created":"2019-02-14T12:25:47Z","quality_controlled":"1","page":"2674-2686","date_updated":"2023-09-19T14:30:23Z","file":[{"file_name":"2018_ASCB_Dolati.pdf","file_id":"5994","content_type":"application/pdf","date_created":"2019-02-14T12:34:29Z","date_updated":"2020-07-14T12:47:15Z","access_level":"open_access","relation":"main_file","checksum":"e98465b4416b3e804c47f40086932af2","file_size":6668971,"creator":"kschuh"}],"isi":1,"volume":29,"article_processing_charge":"No","tmp":{"short":"CC BY-NC-SA (4.0)","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)"},"publication_identifier":{"eissn":["1939-4586"]},"pmid":1,"scopus_import":"1","doi":"10.1091/mbc.e18-02-0082","publisher":"American Society for Cell Biology ","language":[{"iso":"eng"}],"type":"journal_article","file_date_updated":"2020-07-14T12:47:15Z","oa_version":"Published Version","external_id":{"isi":["000455641000011"],"pmid":["30156465"]},"date_published":"2018-11-01T00:00:00Z","issue":"22","publication":"Molecular Biology of the Cell","author":[{"last_name":"Dolati","first_name":"Setareh","full_name":"Dolati, Setareh"},{"last_name":"Kage","first_name":"Frieda","full_name":"Kage, Frieda"},{"first_name":"Jan","full_name":"Mueller, Jan","last_name":"Mueller"},{"last_name":"Müsken","full_name":"Müsken, Mathias","first_name":"Mathias"},{"last_name":"Kirchner","first_name":"Marieluise","full_name":"Kirchner, Marieluise"},{"full_name":"Dittmar, Gunnar","first_name":"Gunnar","last_name":"Dittmar"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","first_name":"Michael K","full_name":"Sixt, Michael K","last_name":"Sixt"},{"last_name":"Rottner","full_name":"Rottner, Klemens","first_name":"Klemens"},{"last_name":"Falcke","full_name":"Falcke, Martin","first_name":"Martin"}],"ddc":["570"]},{"file_date_updated":"2020-07-14T12:47:28Z","type":"journal_article","language":[{"iso":"eng"}],"publisher":"Bio-Protocol","doi":"10.21769/bioprotoc.3018","ddc":["570"],"author":[{"first_name":"Shuxia","full_name":"Fan, Shuxia","last_name":"Fan"},{"full_name":"Lorenz, Michael","first_name":"Michael","last_name":"Lorenz"},{"first_name":"Steffen","full_name":"Massberg, Steffen","last_name":"Massberg"},{"id":"397A88EE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6120-3723","first_name":"Florian R","full_name":"Gärtner, Florian R","last_name":"Gärtner"}],"publication":"Bio-Protocol","issue":"18","date_published":"2018-09-20T00:00:00Z","oa_version":"Published Version","volume":8,"file":[{"relation":"main_file","checksum":"d4588377e789da7f360b553ae02c5119","file_size":2928337,"creator":"dernst","file_name":"2018_BioProtocol_Fan.pdf","date_created":"2019-04-30T08:04:33Z","content_type":"application/pdf","file_id":"6360","date_updated":"2020-07-14T12:47:28Z","access_level":"open_access"}],"date_updated":"2021-01-12T08:07:12Z","project":[{"name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","grant_number":"747687","_id":"260AA4E2-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}],"quality_controlled":"1","date_created":"2019-04-29T09:40:33Z","year":"2018","publication_identifier":{"issn":["2331-8325"]},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"oa":1,"title":"Platelet migration and bacterial trapping assay under flow","publication_status":"published","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","month":"09","_id":"6354","department":[{"_id":"MiSi"}],"acknowledgement":" FöFoLe project 947 (F.G.), the Friedrich-Baur-Stiftung project 41/16 (F.G.)","abstract":[{"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.","lang":"eng"}],"article_number":"e3018","status":"public","ec_funded":1,"intvolume":"         8","citation":{"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>.","ista":"Fan S, Lorenz M, Massberg S, Gärtner FR. 2018. Platelet migration and bacterial trapping assay under flow. Bio-Protocol. 8(18), e3018.","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>","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.","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).","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>"},"keyword":["Platelets","Cell migration","Bacteria","Shear flow","Fibrinogen","E. coli"],"has_accepted_license":"1","day":"20"},{"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","month":"06","_id":"6497","title":"The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells","oa":1,"publication_status":"published","department":[{"_id":"MiSi"}],"status":"public","abstract":[{"text":"T cells are actively scanning pMHC-presenting cells in lymphoid organs and nonlymphoid tissues (NLTs) with divergent topologies and confinement. How the T cell actomyosin cytoskeleton facilitates this task in distinct environments is incompletely understood. Here, we show that lack of Myosin IXb (Myo9b), a negative regulator of the small GTPase Rho, led to increased Rho-GTP levels and cell surface stiffness in primary T cells. Nonetheless, intravital imaging revealed robust motility of Myo9b−/− CD8+ T cells in lymphoid tissue and similar expansion and differentiation during immune responses. In contrast, accumulation of Myo9b−/− CD8+ T cells in NLTs was strongly impaired. Specifically, Myo9b was required for T cell crossing of basement membranes, such as those which are present between dermis and epidermis. As consequence, Myo9b−/− CD8+ T cells showed impaired control of skin infections. In sum, we show that Myo9b is critical for the CD8+ T cell adaptation from lymphoid to NLT surveillance and the establishment of protective tissue–resident T cell populations.","lang":"eng"}],"day":"06","has_accepted_license":"1","intvolume":"      2015","citation":{"chicago":"Moalli, Federica, Xenia Ficht, Philipp Germann, Mykhailo Vladymyrov, Bettina Stolp, Ingrid de Vries, Ruth Lyck, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” <i>The Journal of Experimental Medicine</i>. Rockefeller University Press, 2018. <a href=\"https://doi.org/10.1084/jem.20170896\">https://doi.org/10.1084/jem.20170896</a>.","ista":"Moalli F, Ficht X, Germann P, Vladymyrov M, Stolp B, de Vries I, Lyck R, Balmer J, Fiocchi A, Kreutzfeldt M, Merkler D, Iannacone M, Ariga A, Stoffel MH, Sharpe J, Bähler M, Sixt MK, Diz-Muñoz A, Stein JV. 2018. The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine. 2015(7), 1869–1890.","apa":"Moalli, F., Ficht, X., Germann, P., Vladymyrov, M., Stolp, B., de Vries, I., … Stein, J. V. (2018). The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. <i>The Journal of Experimental Medicine</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1084/jem.20170896\">https://doi.org/10.1084/jem.20170896</a>","ieee":"F. Moalli <i>et al.</i>, “The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells,” <i>The Journal of Experimental Medicine</i>, vol. 2015, no. 7. Rockefeller University Press, pp. 1869–1890, 2018.","mla":"Moalli, Federica, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” <i>The Journal of Experimental Medicine</i>, vol. 2015, no. 7, Rockefeller University Press, 2018, pp. 1869–1890, doi:<a href=\"https://doi.org/10.1084/jem.20170896\">10.1084/jem.20170896</a>.","short":"F. Moalli, X. Ficht, P. Germann, M. Vladymyrov, B. Stolp, I. de Vries, R. Lyck, J. Balmer, A. Fiocchi, M. Kreutzfeldt, D. Merkler, M. Iannacone, A. Ariga, M.H. Stoffel, J. Sharpe, M. Bähler, M.K. Sixt, A. Diz-Muñoz, J.V. Stein, The Journal of Experimental Medicine 2015 (2018) 1869–1890.","ama":"Moalli F, Ficht X, Germann P, et al. The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. <i>The Journal of Experimental Medicine</i>. 2018;2015(7):1869–1890. doi:<a href=\"https://doi.org/10.1084/jem.20170896\">10.1084/jem.20170896</a>"},"doi":"10.1084/jem.20170896","publisher":"Rockefeller University Press","language":[{"iso":"eng"}],"file_date_updated":"2020-07-14T12:47:32Z","type":"journal_article","external_id":{"isi":["000440822900011"]},"oa_version":"Published Version","date_published":"2018-06-06T00:00:00Z","issue":"7","publication":"The Journal of Experimental Medicine","ddc":["570"],"author":[{"first_name":"Federica","full_name":"Moalli, Federica","last_name":"Moalli"},{"last_name":"Ficht","first_name":"Xenia","full_name":"Ficht, Xenia"},{"last_name":"Germann","full_name":"Germann, Philipp","first_name":"Philipp"},{"last_name":"Vladymyrov","first_name":"Mykhailo","full_name":"Vladymyrov, Mykhailo"},{"full_name":"Stolp, Bettina","first_name":"Bettina","last_name":"Stolp"},{"id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid","full_name":"de Vries, Ingrid","last_name":"de Vries"},{"last_name":"Lyck","first_name":"Ruth","full_name":"Lyck, Ruth"},{"last_name":"Balmer","first_name":"Jasmin","full_name":"Balmer, Jasmin"},{"last_name":"Fiocchi","full_name":"Fiocchi, Amleto","first_name":"Amleto"},{"last_name":"Kreutzfeldt","first_name":"Mario","full_name":"Kreutzfeldt, Mario"},{"full_name":"Merkler, Doron","first_name":"Doron","last_name":"Merkler"},{"full_name":"Iannacone, Matteo","first_name":"Matteo","last_name":"Iannacone"},{"last_name":"Ariga","first_name":"Akitaka","full_name":"Ariga, Akitaka"},{"last_name":"Stoffel","full_name":"Stoffel, Michael H.","first_name":"Michael H."},{"full_name":"Sharpe, James","first_name":"James","last_name":"Sharpe"},{"last_name":"Bähler","full_name":"Bähler, Martin","first_name":"Martin"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","last_name":"Sixt","full_name":"Sixt, Michael K","first_name":"Michael K"},{"full_name":"Diz-Muñoz, Alba","first_name":"Alba","last_name":"Diz-Muñoz"},{"first_name":"Jens V.","full_name":"Stein, Jens V.","last_name":"Stein"}],"page":"1869–1890","quality_controlled":"1","date_created":"2019-05-28T12:36:47Z","year":"2018","date_updated":"2023-09-19T14:52:08Z","volume":2015,"isi":1,"file":[{"relation":"main_file","checksum":"86ae5331f9bfced9a6358a790a04bef4","file_size":3841660,"creator":"kschuh","file_name":"2018_rupress_Moalli.pdf","content_type":"application/pdf","date_created":"2019-05-28T12:40:05Z","file_id":"6498","access_level":"open_access","date_updated":"2020-07-14T12:47:32Z"}],"article_processing_charge":"No","tmp":{"short":"CC BY-NC-SA (4.0)","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)"},"publication_identifier":{"issn":["0022-1007"],"eissn":["1540-9538"]},"scopus_import":"1"},{"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>","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.","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>.","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.","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>.","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>"},"intvolume":"       217","day":"12","has_accepted_license":"1","status":"public","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."}],"ec_funded":1,"department":[{"_id":"MiSi"},{"_id":"Bio"}],"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).","title":"Lymphatic exosomes promote dendritic cell migration along guidance cues","oa":1,"publication_status":"published","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","_id":"275","month":"04","scopus_import":"1","pmid":1,"article_processing_charge":"No","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"volume":217,"isi":1,"file":[{"date_created":"2018-12-17T12:50:07Z","content_type":"application/pdf","file_id":"5704","date_updated":"2020-07-14T12:45:45Z","access_level":"open_access","file_name":"2018_JournalCellBiology_Brown.pdf","file_size":2252043,"creator":"dernst","relation":"main_file","checksum":"9c7eba51a35c62da8c13f98120b64df4"}],"page":"2205 - 2221","quality_controlled":"1","year":"2018","date_created":"2018-12-11T11:45:33Z","date_updated":"2023-09-13T08:51:29Z","project":[{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and transduction of leukocytes (FWF)","grant_number":"Y 564-B12","call_identifier":"FWF"},{"call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556","_id":"25A603A2-B435-11E9-9278-68D0E5697425"}],"publication":"Journal of Cell Biology","issue":"6","publist_id":"7627","ddc":["570"],"author":[{"last_name":"Brown","full_name":"Brown, Markus","first_name":"Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Johnson","full_name":"Johnson, Louise","first_name":"Louise"},{"last_name":"Leone","first_name":"Dario","full_name":"Leone, Dario"},{"last_name":"Májek","full_name":"Májek, Peter","first_name":"Peter"},{"orcid":"0000-0001-7829-3518","id":"368EE576-F248-11E8-B48F-1D18A9856A87","full_name":"Vaahtomeri, Kari","first_name":"Kari","last_name":"Vaahtomeri"},{"full_name":"Senfter, Daniel","first_name":"Daniel","last_name":"Senfter"},{"full_name":"Bukosza, Nora","first_name":"Nora","last_name":"Bukosza"},{"first_name":"Helga","full_name":"Schachner, Helga","last_name":"Schachner"},{"last_name":"Asfour","full_name":"Asfour, Gabriele","first_name":"Gabriele"},{"last_name":"Langer","first_name":"Brigitte","full_name":"Langer, Brigitte"},{"full_name":"Hauschild, Robert","first_name":"Robert","last_name":"Hauschild","orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Parapatics","first_name":"Katja","full_name":"Parapatics, Katja"},{"full_name":"Hong, Young","first_name":"Young","last_name":"Hong"},{"first_name":"Keiryn","full_name":"Bennett, Keiryn","last_name":"Bennett"},{"last_name":"Kain","first_name":"Renate","full_name":"Kain, Renate"},{"full_name":"Detmar, Michael","first_name":"Michael","last_name":"Detmar"},{"last_name":"Sixt","full_name":"Sixt, Michael K","first_name":"Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Jackson","first_name":"David","full_name":"Jackson, David"},{"full_name":"Kerjaschki, Dontscho","first_name":"Dontscho","last_name":"Kerjaschki"}],"external_id":{"pmid":["29650776"],"isi":["000438077800026"]},"oa_version":"Published Version","date_published":"2018-04-12T00:00:00Z","language":[{"iso":"eng"}],"file_date_updated":"2020-07-14T12:45:45Z","type":"journal_article","doi":"10.1083/jcb.201612051","publisher":"Rockefeller University Press"},{"oa":1,"title":"Nano-scale microfluidics to study 3D chemotaxis at the single cell level","publication_status":"published","article_type":"original","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","month":"06","_id":"276","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.","department":[{"_id":"MiSi"}],"article_number":"e0198330","status":"public","abstract":[{"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.","lang":"eng"}],"intvolume":"        13","citation":{"short":"C. Frick, P. Dettinger, J. Renkawitz, A. Jauch, C. Berger, M. Recher, T. Schroeder, M. Mehling, PLoS One 13 (2018).","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>","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.","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>.","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>","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>.","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."},"day":"07","has_accepted_license":"1","language":[{"iso":"eng"}],"file_date_updated":"2020-07-14T12:45:45Z","type":"journal_article","doi":"10.1371/journal.pone.0198330","publisher":"Public Library of Science","issue":"6","publist_id":"7626","publication":"PLoS One","ddc":["570"],"author":[{"last_name":"Frick","full_name":"Frick, Corina","first_name":"Corina"},{"full_name":"Dettinger, Philip","first_name":"Philip","last_name":"Dettinger"},{"full_name":"Renkawitz, Jörg","first_name":"Jörg","last_name":"Renkawitz","orcid":"0000-0003-2856-3369","id":"3F0587C8-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Jauch, Annaïse","first_name":"Annaïse","last_name":"Jauch"},{"first_name":"Christoph","full_name":"Berger, Christoph","last_name":"Berger"},{"last_name":"Recher","first_name":"Mike","full_name":"Recher, Mike"},{"full_name":"Schroeder, Timm","first_name":"Timm","last_name":"Schroeder"},{"first_name":"Matthias","full_name":"Mehling, Matthias","last_name":"Mehling"}],"external_id":{"isi":["000434384900031"]},"oa_version":"Published Version","date_published":"2018-06-07T00:00:00Z","volume":13,"isi":1,"file":[{"access_level":"open_access","date_updated":"2020-07-14T12:45:45Z","content_type":"application/pdf","date_created":"2018-12-17T14:10:32Z","file_id":"5709","file_name":"2018_Plos_Frick.pdf","creator":"dernst","file_size":7682167,"checksum":"95fc5dc3938b3ad3b7697d10c83cc143","relation":"main_file"}],"quality_controlled":"1","year":"2018","date_created":"2018-12-11T11:45:34Z","date_updated":"2023-09-13T09:00:15Z","scopus_import":"1","article_processing_charge":"No","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"}}]