[{"department":[{"_id":"MiSi"}],"date_updated":"2023-08-30T07:22:20Z","status":"public","type":"journal_article","article_type":"review","_id":"7009","issue":"12","volume":20,"language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"eissn":["1471-0080"],"issn":["1471-0072"]},"intvolume":" 20","month":"12","scopus_import":"1","pmid":1,"oa_version":"None","abstract":[{"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.","lang":"eng"}],"title":"Mechanisms of 3D cell migration","article_processing_charge":"No","external_id":{"isi":["000497966900007"],"pmid":["31582855"]},"author":[{"first_name":"KM","last_name":"Yamada","full_name":"Yamada, KM"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"chicago":"Yamada, KM, and Michael K Sixt. “Mechanisms of 3D Cell Migration.” Nature Reviews Molecular Cell Biology. Springer Nature, 2019. https://doi.org/10.1038/s41580-019-0172-9.","ista":"Yamada K, Sixt MK. 2019. Mechanisms of 3D cell migration. Nature Reviews Molecular Cell Biology. 20(12), 738–752.","mla":"Yamada, KM, and Michael K. Sixt. “Mechanisms of 3D Cell Migration.” Nature Reviews Molecular Cell Biology, vol. 20, no. 12, Springer Nature, 2019, pp. 738–752, doi:10.1038/s41580-019-0172-9.","apa":"Yamada, K., & Sixt, M. K. (2019). Mechanisms of 3D cell migration. Nature Reviews Molecular Cell Biology. Springer Nature. https://doi.org/10.1038/s41580-019-0172-9","ama":"Yamada K, Sixt MK. Mechanisms of 3D cell migration. Nature Reviews Molecular Cell Biology. 2019;20(12):738–752. doi:10.1038/s41580-019-0172-9","short":"K. Yamada, M.K. Sixt, Nature Reviews Molecular Cell Biology 20 (2019) 738–752.","ieee":"K. Yamada and M. K. Sixt, “Mechanisms of 3D cell migration,” Nature Reviews Molecular Cell Biology, vol. 20, no. 12. Springer Nature, pp. 738–752, 2019."},"date_created":"2019-11-12T14:54:42Z","doi":"10.1038/s41580-019-0172-9","date_published":"2019-12-01T00:00:00Z","page":"738–752","publication":"Nature Reviews Molecular Cell Biology","day":"01","year":"2019","isi":1,"quality_controlled":"1","publisher":"Springer Nature"},{"page":"922-938","date_published":"2019-10-01T00:00:00Z","doi":"10.1016/j.it.2019.08.004","date_created":"2019-11-04T16:27:36Z","isi":1,"year":"2019","day":"01","publication":"Trends in Immunology","quality_controlled":"1","publisher":"Cell Press","author":[{"first_name":"Leo","last_name":"Nicolai","full_name":"Nicolai, Leo"},{"first_name":"Florian R","id":"397A88EE-F248-11E8-B48F-1D18A9856A87","full_name":"Gärtner, Florian R","orcid":"0000-0001-6120-3723","last_name":"Gärtner"},{"first_name":"Steffen","last_name":"Massberg","full_name":"Massberg, Steffen"}],"article_processing_charge":"No","external_id":{"pmid":["31601520"],"isi":["000493292100005"]},"title":"Platelets in host defense: Experimental and clinical insights","citation":{"apa":"Nicolai, L., Gärtner, F. R., & Massberg, S. (2019). Platelets in host defense: Experimental and clinical insights. Trends in Immunology. Cell Press. https://doi.org/10.1016/j.it.2019.08.004","ama":"Nicolai L, Gärtner FR, Massberg S. Platelets in host defense: Experimental and clinical insights. Trends in Immunology. 2019;40(10):922-938. doi:10.1016/j.it.2019.08.004","ieee":"L. Nicolai, F. R. Gärtner, and S. Massberg, “Platelets in host defense: Experimental and clinical insights,” Trends in Immunology, vol. 40, no. 10. Cell Press, pp. 922–938, 2019.","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.” Trends in Immunology, vol. 40, no. 10, Cell Press, 2019, pp. 922–38, doi:10.1016/j.it.2019.08.004.","ista":"Nicolai L, Gärtner FR, Massberg S. 2019. Platelets in host defense: Experimental and clinical insights. Trends in Immunology. 40(10), 922–938.","chicago":"Nicolai, Leo, Florian R Gärtner, and Steffen Massberg. “Platelets in Host Defense: Experimental and Clinical Insights.” Trends in Immunology. Cell Press, 2019. https://doi.org/10.1016/j.it.2019.08.004."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","project":[{"call_identifier":"H2020","_id":"260AA4E2-B435-11E9-9278-68D0E5697425","name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","grant_number":"747687"}],"issue":"10","volume":40,"ec_funded":1,"publication_identifier":{"issn":["1471-4906"]},"publication_status":"published","language":[{"iso":"eng"}],"scopus_import":"1","month":"10","intvolume":" 40","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"}],"oa_version":"None","pmid":1,"department":[{"_id":"MiSi"}],"date_updated":"2023-08-30T07:19:23Z","article_type":"review","type":"journal_article","status":"public","_id":"6988"},{"title":"Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal","external_id":{"pmid":["31639357"],"isi":["000491286200016"]},"article_processing_charge":"No","author":[{"last_name":"Kopf","full_name":"Kopf, Aglaja","orcid":"0000-0002-2187-6656","id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87","first_name":"Aglaja"},{"full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"mla":"Kopf, Aglaja, and Michael K. Sixt. “Gut Homeostasis: Active Migration of Intestinal Epithelial Cells in Tissue Renewal.” Current Biology, vol. 29, no. 20, Cell Press, 2019, pp. R1091–93, doi:10.1016/j.cub.2019.08.068.","short":"A. Kopf, M.K. Sixt, Current Biology 29 (2019) R1091–R1093.","ieee":"A. Kopf and M. K. Sixt, “Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal,” Current Biology, vol. 29, no. 20. Cell Press, pp. R1091–R1093, 2019.","ama":"Kopf A, Sixt MK. Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal. Current Biology. 2019;29(20):R1091-R1093. doi:10.1016/j.cub.2019.08.068","apa":"Kopf, A., & Sixt, M. K. (2019). Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2019.08.068","chicago":"Kopf, Aglaja, and Michael K Sixt. “Gut Homeostasis: Active Migration of Intestinal Epithelial Cells in Tissue Renewal.” Current Biology. Cell Press, 2019. https://doi.org/10.1016/j.cub.2019.08.068.","ista":"Kopf A, Sixt MK. 2019. Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal. Current Biology. 29(20), R1091–R1093."},"publisher":"Cell Press","quality_controlled":"1","date_created":"2019-11-04T15:18:29Z","date_published":"2019-10-21T00:00:00Z","doi":"10.1016/j.cub.2019.08.068","page":"R1091-R1093","publication":"Current Biology","day":"21","year":"2019","isi":1,"status":"public","type":"journal_article","article_type":"original","_id":"6979","department":[{"_id":"MiSi"}],"date_updated":"2023-09-05T12:43:43Z","intvolume":" 29","month":"10","scopus_import":"1","pmid":1,"oa_version":"None","issue":"20","volume":29,"language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"eissn":["1879-0445"],"issn":["0960-9822"]}},{"issue":"11","volume":21,"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["1476-4679"],"issn":["1465-7392"]},"publication_status":"published","month":"11","intvolume":" 21","scopus_import":"1","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7025891","open_access":"1"}],"oa_version":"Submitted Version","pmid":1,"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."}],"department":[{"_id":"MiSi"}],"date_updated":"2023-09-06T11:08:52Z","status":"public","type":"journal_article","article_type":"original","_id":"7105","doi":"10.1038/s41556-019-0411-5","date_published":"2019-11-01T00:00:00Z","date_created":"2019-11-25T08:55:00Z","page":"1370-1381","day":"01","publication":"Nature Cell Biology","isi":1,"year":"2019","quality_controlled":"1","publisher":"Springer Nature","oa":1,"title":"Persistent and polarized global actin flow is essential for directionality during cell migration","author":[{"last_name":"Yolland","full_name":"Yolland, Lawrence","first_name":"Lawrence"},{"full_name":"Burki, Mubarik","last_name":"Burki","first_name":"Mubarik"},{"first_name":"Stefania","last_name":"Marcotti","full_name":"Marcotti, Stefania"},{"first_name":"Andrei","last_name":"Luchici","full_name":"Luchici, Andrei"},{"first_name":"Fiona N.","full_name":"Kenny, Fiona N.","last_name":"Kenny"},{"last_name":"Davis","full_name":"Davis, John Robert","first_name":"John Robert"},{"full_name":"Serna-Morales, Eduardo","last_name":"Serna-Morales","first_name":"Eduardo"},{"id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","first_name":"Jan","full_name":"Müller, Jan","last_name":"Müller"},{"full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Davidson","full_name":"Davidson, Andrew","first_name":"Andrew"},{"last_name":"Wood","full_name":"Wood, Will","first_name":"Will"},{"full_name":"Schumacher, Linus J.","last_name":"Schumacher","first_name":"Linus J."},{"first_name":"Robert G.","full_name":"Endres, Robert G.","last_name":"Endres"},{"first_name":"Mark","full_name":"Miodownik, Mark","last_name":"Miodownik"},{"last_name":"Stramer","full_name":"Stramer, Brian M.","first_name":"Brian M."}],"external_id":{"pmid":["31685997"],"isi":["000495888300009"]},"article_processing_charge":"No","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","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. Nature Cell Biology. Springer Nature. https://doi.org/10.1038/s41556-019-0411-5","ama":"Yolland L, Burki M, Marcotti S, et al. Persistent and polarized global actin flow is essential for directionality during cell migration. Nature Cell Biology. 2019;21(11):1370-1381. doi:10.1038/s41556-019-0411-5","ieee":"L. Yolland et al., “Persistent and polarized global actin flow is essential for directionality during cell migration,” Nature Cell Biology, vol. 21, no. 11. Springer Nature, pp. 1370–1381, 2019.","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.","mla":"Yolland, Lawrence, et al. “Persistent and Polarized Global Actin Flow Is Essential for Directionality during Cell Migration.” Nature Cell Biology, vol. 21, no. 11, Springer Nature, 2019, pp. 1370–81, doi:10.1038/s41556-019-0411-5.","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.” Nature Cell Biology. Springer Nature, 2019. https://doi.org/10.1038/s41556-019-0411-5."}},{"pmid":1,"oa_version":"Published Version","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"}],"month":"06","intvolume":" 132","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1242/jcs.233387"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0021-9533"],"eissn":["1477-9137"]},"publication_status":"published","issue":"11","volume":132,"_id":"7420","status":"public","type":"journal_article","article_type":"original","date_updated":"2023-09-06T15:01:00Z","department":[{"_id":"MiSi"}],"quality_controlled":"1","publisher":"The Company of Biologists","oa":1,"day":"07","publication":"Journal of Cell Science","isi":1,"year":"2019","doi":"10.1242/jcs.233387","date_published":"2019-06-07T00:00:00Z","date_created":"2020-01-30T10:31:42Z","article_number":"jcs233387","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"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.","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.” Journal of Cell Science. The Company of Biologists, 2019. https://doi.org/10.1242/jcs.233387.","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).","ieee":"P. Sahgal et al., “GGA2 and RAB13 promote activity-dependent β1-integrin recycling,” Journal of Cell Science, vol. 132, no. 11. The Company of Biologists, 2019.","ama":"Sahgal P, Alanko JH, Icha J, et al. GGA2 and RAB13 promote activity-dependent β1-integrin recycling. Journal of Cell Science. 2019;132(11). doi:10.1242/jcs.233387","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. Journal of Cell Science. The Company of Biologists. https://doi.org/10.1242/jcs.233387","mla":"Sahgal, Pranshu, et al. “GGA2 and RAB13 Promote Activity-Dependent Β1-Integrin Recycling.” Journal of Cell Science, vol. 132, no. 11, jcs233387, The Company of Biologists, 2019, doi:10.1242/jcs.233387."},"title":"GGA2 and RAB13 promote activity-dependent β1-integrin recycling","author":[{"first_name":"Pranshu","full_name":"Sahgal, Pranshu","last_name":"Sahgal"},{"first_name":"Jonna H","id":"2CC12E8C-F248-11E8-B48F-1D18A9856A87","full_name":"Alanko, Jonna H","orcid":"0000-0002-7698-3061","last_name":"Alanko"},{"first_name":"Jaroslav","last_name":"Icha","full_name":"Icha, Jaroslav"},{"last_name":"Paatero","full_name":"Paatero, Ilkka","first_name":"Ilkka"},{"first_name":"Hellyeh","full_name":"Hamidi, Hellyeh","last_name":"Hamidi"},{"last_name":"Arjonen","full_name":"Arjonen, Antti","first_name":"Antti"},{"first_name":"Mika","full_name":"Pietilä, Mika","last_name":"Pietilä"},{"last_name":"Rokka","full_name":"Rokka, Anne","first_name":"Anne"},{"full_name":"Ivaska, Johanna","last_name":"Ivaska","first_name":"Johanna"}],"external_id":{"isi":["000473327900017"],"pmid":["31076515"]},"article_processing_charge":"No"},{"date_updated":"2023-09-07T14:47:00Z","department":[{"_id":"MiSi"}],"_id":"7404","status":"public","type":"journal_article","article_type":"original","language":[{"iso":"eng"}],"publication_status":"published","publication_identifier":{"eissn":["1477-9129"],"issn":["0950-1991"]},"volume":146,"issue":"7","pmid":1,"oa_version":"Published Version","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"}],"intvolume":" 146","month":"04","main_file_link":[{"url":"https://doi.org/10.1242/dev.171397","open_access":"1"}],"scopus_import":"1","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"mla":"Stürner, Tomke, et al. “Transient Localization of the Arp2/3 Complex Initiates Neuronal Dendrite Branching in Vivo.” Development, vol. 146, no. 7, dev171397, The Company of Biologists, 2019, doi:10.1242/dev.171397.","short":"T. Stürner, A. Tatarnikova, J. Müller, B. Schaffran, H. Cuntz, Y. Zhang, M. Nemethova, S. Bogdan, V. Small, G. Tavosanis, Development 146 (2019).","ieee":"T. Stürner et al., “Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo,” Development, vol. 146, no. 7. The Company of Biologists, 2019.","ama":"Stürner T, Tatarnikova A, Müller J, et al. Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo. Development. 2019;146(7). doi:10.1242/dev.171397","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. Development. The Company of Biologists. https://doi.org/10.1242/dev.171397","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.” Development. The Company of Biologists, 2019. https://doi.org/10.1242/dev.171397.","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."},"title":"Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo","external_id":{"pmid":["30910826"],"isi":["000464583200006"]},"article_processing_charge":"No","author":[{"first_name":"Tomke","full_name":"Stürner, Tomke","last_name":"Stürner"},{"first_name":"Anastasia","last_name":"Tatarnikova","full_name":"Tatarnikova, Anastasia"},{"last_name":"Müller","full_name":"Müller, Jan","id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","first_name":"Jan"},{"full_name":"Schaffran, Barbara","last_name":"Schaffran","first_name":"Barbara"},{"last_name":"Cuntz","full_name":"Cuntz, Hermann","first_name":"Hermann"},{"last_name":"Zhang","full_name":"Zhang, Yun","first_name":"Yun"},{"last_name":"Nemethova","full_name":"Nemethova, Maria","first_name":"Maria","id":"34E27F1C-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Bogdan","full_name":"Bogdan, Sven","first_name":"Sven"},{"full_name":"Small, Vic","last_name":"Small","first_name":"Vic"},{"first_name":"Gaia","full_name":"Tavosanis, Gaia","last_name":"Tavosanis"}],"article_number":"dev171397","publication":"Development","day":"04","year":"2019","isi":1,"date_created":"2020-01-29T16:27:10Z","doi":"10.1242/dev.171397","date_published":"2019-04-04T00:00:00Z","oa":1,"quality_controlled":"1","publisher":"The Company of Biologists"},{"title":"Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking","article_processing_charge":"No","author":[{"orcid":"0000-0003-3470-6119","full_name":"Assen, Frank P","last_name":"Assen","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","first_name":"Frank P"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"chicago":"Assen, Frank P. “Lymph Node Mechanics: Deciphering the Interplay between Stroma Contractility, Morphology and Lymphocyte Trafficking.” Institute of Science and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6947.","ista":"Assen FP. 2019. Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking. Institute of Science and Technology Austria.","mla":"Assen, Frank P. Lymph Node Mechanics: Deciphering the Interplay between Stroma Contractility, Morphology and Lymphocyte Trafficking. Institute of Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:6947.","ieee":"F. P. Assen, “Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking,” Institute of Science and Technology Austria, 2019.","short":"F.P. Assen, Lymph Node Mechanics: Deciphering the Interplay between Stroma Contractility, Morphology and Lymphocyte Trafficking, Institute of Science and Technology Austria, 2019.","ama":"Assen FP. Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking. 2019. doi:10.15479/AT:ISTA:6947","apa":"Assen, F. P. (2019). Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:6947"},"oa":1,"publisher":"Institute of Science and Technology Austria","date_created":"2019-10-14T16:54:52Z","date_published":"2019-10-09T00:00:00Z","doi":"10.15479/AT:ISTA:6947","page":"142","day":"9","year":"2019","has_accepted_license":"1","status":"public","type":"dissertation","_id":"6947","department":[{"_id":"MiSi"}],"file_date_updated":"2020-11-07T23:30:03Z","ddc":["570"],"date_updated":"2023-09-13T08:50:57Z","supervisor":[{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"month":"10","alternative_title":["ISTA Thesis"],"oa_version":"Published Version","abstract":[{"lang":"eng","text":"Lymph nodes are es s ential organs of the immune s ys tem where adaptive immune responses originate, and consist of various leukocyte populations and a stromal backbone. Fibroblastic reticular cells (FRCs) are the main stromal cells and form a sponge-like extracellular matrix network, called conduits , which they thems elves enwrap and contract. Lymph, containing s oluble antigens , arrive in lymph nodes via afferent lymphatic vessels that connect to the s ubcaps ular s inus and conduit network. According to the current paradigm, the conduit network dis tributes afferent lymph through lymph nodes and thus provides acces s for immune cells to lymph-borne antigens. An elas tic caps ule s urrounds the organ and confines the immune cells and FRC network. Lymph nodes are completely packed with lymphocytes and lymphocyte numbers directly dictates the size of the organ. Although lymphocytes cons tantly enter and leave the lymph node, its s ize remains remarkedly s table under homeostatic conditions. It is only partly known how the cellularity and s ize of the lymph node is regulated and how the lymph node is able to swell in inflammation. The role of the FRC network in lymph node s welling and trans fer of fluids are inves tigated in this thes is. Furthermore, we s tudied what trafficking routes are us ed by cancer cells in lymph nodes to form distal metastases.We examined the role of a mechanical feedback in regulation of lymph node swelling. Using parallel plate compression and UV-las er cutting experiments we dis s ected the mechanical force dynamics of the whole lymph node, and individually for FRCs and the caps ule. Physical forces generated by packed lymphocytes directly affect the tens ion on the FRC network and capsule, which increases its resistance to swelling. This implies a feedback mechanism between tis s ue pres s ure and ability of lymphocytes to enter the organ. Following inflammation, the lymph node swells ∼10 fold in two weeks . Yet, what is the role for tens ion on the FRC network and caps ule, and how are lymphocytes able to enter in conditions that resist swelling remain open ques tions . We s how that tens ion on the FRC network is important to limit the swelling rate of the organ so that the FRC network can grow in a coordinated fashion. This is illustrated by interfering with FRC contractility, which leads to faster swelling rates and a dis organized FRC network in the inflamed lymph node. Growth of the FRC network in turn is expected to releas e tens ion on thes e s tructures and lowers the res is tance to swelling, thereby allowing more lymphocytes to enter the organ and drive more swelling. Halt of swelling coincides with a thickening of the caps ule, which forms a thick res is tant band around the organ and lowers tens ion on the FRC network to form a new force equilibrium.The FRC and conduit network are further believed to be a privileged s ite of s oluble information within the lymph node, although many details remain uns olved. We s how by 3D ultra-recons truction that FRCs and antigen pres enting cells cover the s urface of conduit s ys tem for more than 99% and we dis cus s the implications for s oluble information exchangeat the conduit level.Finally, there is an ongoing debate in the cancer field whether and how cancer cells in lymph nodes s eed dis tal metas tas es . We s how that cancer cells infus ed into the lymph node can utilize trafficking routes of immune cells and rapidly migrate to blood vessels. Once in the blood circulation, these cells are able to form metastases in distal tissues."}],"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"},{"_id":"EM-Fac"}],"related_material":{"record":[{"relation":"part_of_dissertation","id":"664","status":"public"},{"status":"public","id":"402","relation":"part_of_dissertation"}]},"language":[{"iso":"eng"}],"file":[{"file_id":"6990","checksum":"53a739752a500f84d0f8ec953cbbd0b6","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","embargo_to":"open_access","access_level":"closed","relation":"source_file","date_created":"2019-11-06T12:30:02Z","file_name":"PhDthesis_FrankAssen_revised2.docx","date_updated":"2020-11-07T23:30:03Z","file_size":214172667,"creator":"fassen"},{"embargo":"2020-11-06","file_id":"6991","checksum":"8c156b65d9347bb599623a4b09f15d15","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"PhDthesis_FrankAssen_revised2.pdf","date_created":"2019-11-06T12:30:57Z","creator":"fassen","file_size":83637532,"date_updated":"2020-11-07T23:30:03Z"}],"publication_status":"published","degree_awarded":"PhD","publication_identifier":{"issn":["2663-337X"]}},{"title":"The implication of cytoskeletal dynamics on leukocyte migration","author":[{"orcid":"0000-0002-2187-6656","full_name":"Kopf, Aglaja","last_name":"Kopf","first_name":"Aglaja","id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87"}],"article_processing_charge":"No","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","citation":{"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. https://doi.org/10.15479/AT:ISTA:6891.","ieee":"A. Kopf, “The implication of cytoskeletal dynamics on leukocyte migration,” Institute of Science and Technology Austria, 2019.","short":"A. Kopf, The Implication of Cytoskeletal Dynamics on Leukocyte Migration, Institute of Science and Technology Austria, 2019.","ama":"Kopf A. The implication of cytoskeletal dynamics on leukocyte migration. 2019. doi:10.15479/AT:ISTA:6891","apa":"Kopf, A. (2019). The implication of cytoskeletal dynamics on leukocyte migration. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:6891","mla":"Kopf, Aglaja. The Implication of Cytoskeletal Dynamics on Leukocyte Migration. Institute of Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:6891."},"project":[{"name":"Nano-Analytics of Cellular Systems","grant_number":"W01250-B20","_id":"265E2996-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"doi":"10.15479/AT:ISTA:6891","date_published":"2019-07-24T00:00:00Z","date_created":"2019-09-19T08:19:44Z","page":"171","day":"24","has_accepted_license":"1","year":"2019","publisher":"Institute of Science and Technology Austria","oa":1,"file_date_updated":"2020-10-17T22:30:03Z","department":[{"_id":"MiSi"}],"ddc":["570"],"supervisor":[{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"}],"date_updated":"2023-10-18T08:49:17Z","status":"public","keyword":["cell biology","immunology","leukocyte","migration","microfluidics"],"type":"dissertation","_id":"6891","related_material":{"record":[{"relation":"part_of_dissertation","status":"public","id":"6328"},{"id":"15","status":"public","relation":"part_of_dissertation"},{"relation":"part_of_dissertation","id":"6877","status":"public"}],"link":[{"relation":"press_release","url":"https://ist.ac.at/en/news/feeling-like-a-cell/"}]},"file":[{"creator":"akopf","date_updated":"2020-10-17T22:30:03Z","file_size":74735267,"date_created":"2019-10-15T05:28:42Z","file_name":"Kopf_PhD_Thesis.docx","access_level":"closed","relation":"source_file","content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","embargo_to":"open_access","file_id":"6950","checksum":"00d100d6468e31e583051e0a006b640c"},{"date_created":"2019-10-15T05:28:47Z","file_name":"Kopf_PhD_Thesis1.pdf","date_updated":"2020-10-17T22:30:03Z","file_size":52787224,"creator":"akopf","checksum":"5d1baa899993ae6ca81aebebe1797000","file_id":"6951","embargo":"2020-10-16","content_type":"application/pdf","access_level":"open_access","relation":"main_file"}],"language":[{"iso":"eng"}],"publication_identifier":{"isbn":["978-3-99078-002-2"],"eissn":["2663-337X"]},"degree_awarded":"PhD","publication_status":"published","month":"07","alternative_title":["ISTA Thesis"],"oa_version":"Published Version","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"}]},{"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"mla":"Renkawitz, Jörg, et al. “Nuclear Positioning Facilitates Amoeboid Migration along the Path of Least Resistance.” Nature, vol. 568, Springer Nature, 2019, pp. 546–50, doi:10.1038/s41586-019-1087-5.","apa":"Renkawitz, J., Kopf, A., Stopp, J. A., de Vries, I., Driscoll, M. K., Merrin, J., … Sixt, M. K. (2019). Nuclear positioning facilitates amoeboid migration along the path of least resistance. Nature. Springer Nature. https://doi.org/10.1038/s41586-019-1087-5","ama":"Renkawitz J, Kopf A, Stopp JA, et al. Nuclear positioning facilitates amoeboid migration along the path of least resistance. Nature. 2019;568:546-550. doi:10.1038/s41586-019-1087-5","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.","ieee":"J. Renkawitz et al., “Nuclear positioning facilitates amoeboid migration along the path of least resistance,” Nature, vol. 568. Springer Nature, pp. 546–550, 2019.","chicago":"Renkawitz, Jörg, Aglaja Kopf, Julian A Stopp, Ingrid de Vries, Meghan K. Driscoll, Jack Merrin, Robert Hauschild, et al. “Nuclear Positioning Facilitates Amoeboid Migration along the Path of Least Resistance.” Nature. Springer Nature, 2019. https://doi.org/10.1038/s41586-019-1087-5.","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."},"title":"Nuclear positioning facilitates amoeboid migration along the path of least resistance","article_processing_charge":"No","external_id":{"pmid":["30944468"],"isi":["000465594200050"]},"author":[{"id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","first_name":"Jörg","last_name":"Renkawitz","full_name":"Renkawitz, Jörg","orcid":"0000-0003-2856-3369"},{"first_name":"Aglaja","id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87","last_name":"Kopf","full_name":"Kopf, Aglaja","orcid":"0000-0002-2187-6656"},{"first_name":"Julian A","id":"489E3F00-F248-11E8-B48F-1D18A9856A87","last_name":"Stopp","full_name":"Stopp, Julian A"},{"full_name":"de Vries, Ingrid","last_name":"de Vries","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","first_name":"Ingrid"},{"full_name":"Driscoll, Meghan K.","last_name":"Driscoll","first_name":"Meghan K."},{"last_name":"Merrin","full_name":"Merrin, Jack","orcid":"0000-0001-5145-4609","first_name":"Jack","id":"4515C308-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522","last_name":"Hauschild"},{"first_name":"Erik S.","full_name":"Welf, Erik S.","last_name":"Welf"},{"full_name":"Danuser, Gaudenz","last_name":"Danuser","first_name":"Gaudenz"},{"first_name":"Reto","last_name":"Fiolka","full_name":"Fiolka, Reto"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"project":[{"_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","grant_number":"281556"},{"call_identifier":"H2020","_id":"25FE9508-B435-11E9-9278-68D0E5697425","grant_number":"724373","name":"Cellular navigation along spatial gradients"},{"name":"Nano-Analytics of Cellular Systems","grant_number":"W01250-B20","_id":"265FAEBA-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"grant_number":"291734","name":"International IST Postdoc Fellowship Programme","call_identifier":"FP7","_id":"25681D80-B435-11E9-9278-68D0E5697425"},{"name":"Molecular and system level view of immune cell migration","grant_number":"ALTF 1396-2014","_id":"25A48D24-B435-11E9-9278-68D0E5697425"}],"publication":"Nature","day":"25","year":"2019","isi":1,"date_created":"2019-04-17T06:52:28Z","doi":"10.1038/s41586-019-1087-5","date_published":"2019-04-25T00:00:00Z","page":"546-550","oa":1,"publisher":"Springer Nature","quality_controlled":"1","date_updated":"2024-03-27T23:30:39Z","department":[{"_id":"MiSi"},{"_id":"NanoFab"},{"_id":"Bio"}],"_id":"6328","status":"public","article_type":"letter_note","type":"journal_article","language":[{"iso":"eng"}],"publication_status":"published","ec_funded":1,"volume":568,"related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"14697"},{"relation":"dissertation_contains","id":"6891","status":"public"}],"link":[{"description":"News on IST Homepage","relation":"press_release","url":"https://ist.ac.at/en/news/leukocytes-use-their-nucleus-as-a-ruler-to-choose-path-of-least-resistance/"}]},"pmid":1,"oa_version":"Submitted Version","acknowledged_ssus":[{"_id":"SSU"}],"abstract":[{"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.","lang":"eng"}],"intvolume":" 568","month":"04","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217284/","open_access":"1"}],"scopus_import":"1"},{"oa_version":"None","pmid":1,"month":"09","intvolume":" 179","scopus_import":"1","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0092-8674"],"eissn":["1097-4172"]},"publication_status":"published","volume":179,"issue":"1","related_material":{"record":[{"id":"6891","status":"public","relation":"dissertation_contains"}]},"_id":"6877","status":"public","article_type":"original","type":"journal_article","date_updated":"2024-03-27T23:30:40Z","department":[{"_id":"MiSi"}],"quality_controlled":"1","publisher":"Elsevier","day":"19","publication":"Cell","isi":1,"year":"2019","doi":"10.1016/j.cell.2019.08.047","date_published":"2019-09-19T00:00:00Z","date_created":"2019-09-15T22:00:46Z","page":"51-53","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Kopf, Aglaja, and Michael K Sixt. “The Neural Crest Pitches in to Remove Apoptotic Debris.” Cell. Elsevier, 2019. https://doi.org/10.1016/j.cell.2019.08.047.","ista":"Kopf A, Sixt MK. 2019. The neural crest pitches in to remove apoptotic debris. Cell. 179(1), 51–53.","mla":"Kopf, Aglaja, and Michael K. Sixt. “The Neural Crest Pitches in to Remove Apoptotic Debris.” Cell, vol. 179, no. 1, Elsevier, 2019, pp. 51–53, doi:10.1016/j.cell.2019.08.047.","apa":"Kopf, A., & Sixt, M. K. (2019). The neural crest pitches in to remove apoptotic debris. Cell. Elsevier. https://doi.org/10.1016/j.cell.2019.08.047","ama":"Kopf A, Sixt MK. The neural crest pitches in to remove apoptotic debris. Cell. 2019;179(1):51-53. doi:10.1016/j.cell.2019.08.047","ieee":"A. Kopf and M. K. Sixt, “The neural crest pitches in to remove apoptotic debris,” Cell, vol. 179, no. 1. Elsevier, pp. 51–53, 2019.","short":"A. Kopf, M.K. Sixt, Cell 179 (2019) 51–53."},"title":"The neural crest pitches in to remove apoptotic debris","author":[{"first_name":"Aglaja","id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-2187-6656","full_name":"Kopf, Aglaja","last_name":"Kopf"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179"}],"external_id":{"isi":["000486618500011"],"pmid":["31539498"]},"article_processing_charge":"No"}]