{"date_published":"2017-09-21T00:00:00Z","citation":{"apa":"Mueller, J., Szep, G., Nemethova, M., de Vries, I., Lieber, A., Winkler, C., … Sixt, M. K. (2017). Load adaptation of lamellipodial actin networks. Cell. Cell Press. https://doi.org/10.1016/j.cell.2017.07.051","ista":"Mueller J, Szep G, Nemethova M, de Vries I, Lieber A, Winkler C, Kruse K, Small J, Schmeiser C, Keren K, Hauschild R, Sixt MK. 2017. Load adaptation of lamellipodial actin networks. Cell. 171(1), 188–200.","chicago":"Mueller, Jan, Gregory Szep, Maria Nemethova, Ingrid de Vries, Arnon Lieber, Christoph Winkler, Karsten Kruse, et al. “Load Adaptation of Lamellipodial Actin Networks.” Cell. Cell Press, 2017. https://doi.org/10.1016/j.cell.2017.07.051.","ieee":"J. Mueller et al., “Load adaptation of lamellipodial actin networks,” Cell, vol. 171, no. 1. Cell Press, pp. 188–200, 2017.","ama":"Mueller J, Szep G, Nemethova M, et al. Load adaptation of lamellipodial actin networks. Cell. 2017;171(1):188-200. doi:10.1016/j.cell.2017.07.051","mla":"Mueller, Jan, et al. “Load Adaptation of Lamellipodial Actin Networks.” Cell, vol. 171, no. 1, Cell Press, 2017, pp. 188–200, doi:10.1016/j.cell.2017.07.051.","short":"J. Mueller, G. Szep, M. Nemethova, I. de Vries, A. Lieber, C. Winkler, K. Kruse, J. Small, C. Schmeiser, K. Keren, R. Hauschild, M.K. Sixt, Cell 171 (2017) 188–200."},"intvolume":" 171","project":[{"name":"Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments","_id":"25AD6156-B435-11E9-9278-68D0E5697425","grant_number":"LS13-029"},{"_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)","call_identifier":"FP7"}],"title":"Load adaptation of lamellipodial actin networks","quality_controlled":"1","publication_identifier":{"issn":["00928674"]},"year":"2017","month":"09","ec_funded":1,"date_updated":"2023-09-28T11:33:49Z","publist_id":"6951","oa_version":"None","author":[{"first_name":"Jan","last_name":"Mueller","full_name":"Mueller, Jan"},{"id":"4BFB7762-F248-11E8-B48F-1D18A9856A87","full_name":"Szep, Gregory","last_name":"Szep","first_name":"Gregory"},{"id":"34E27F1C-F248-11E8-B48F-1D18A9856A87","full_name":"Nemethova, Maria","last_name":"Nemethova","first_name":"Maria"},{"first_name":"Ingrid","last_name":"De Vries","full_name":"De Vries, Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Lieber","first_name":"Arnon","full_name":"Lieber, Arnon"},{"first_name":"Christoph","last_name":"Winkler","full_name":"Winkler, Christoph"},{"full_name":"Kruse, Karsten","first_name":"Karsten","last_name":"Kruse"},{"last_name":"Small","first_name":"John","full_name":"Small, John"},{"first_name":"Christian","last_name":"Schmeiser","full_name":"Schmeiser, Christian"},{"first_name":"Kinneret","last_name":"Keren","full_name":"Keren, Kinneret"},{"last_name":"Hauschild","orcid":"0000-0001-9843-3522","first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","full_name":"Hauschild, Robert"},{"last_name":"Sixt","orcid":"0000-0002-6620-9179","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K"}],"status":"public","external_id":{"isi":["000411331800020"]},"issue":"1","type":"journal_article","page":"188 - 200","doi":"10.1016/j.cell.2017.07.051","department":[{"_id":"MiSi"},{"_id":"Bio"}],"day":"21","publisher":"Cell Press","acknowledged_ssus":[{"_id":"ScienComp"}],"article_processing_charge":"No","isi":1,"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","abstract":[{"lang":"eng","text":"Actin filaments polymerizing against membranes power endocytosis, vesicular traffic, and cell motility. In vitro reconstitution studies suggest that the structure and the dynamics of actin networks respond to mechanical forces. We demonstrate that lamellipodial actin of migrating cells responds to mechanical load when membrane tension is modulated. In a steady state, migrating cell filaments assume the canonical dendritic geometry, defined by Arp2/3-generated 70° branch points. Increased tension triggers a dense network with a broadened range of angles, whereas decreased tension causes a shift to a sparse configuration dominated by filaments growing perpendicularly to the plasma membrane. We show that these responses emerge from the geometry of branched actin: when load per filament decreases, elongation speed increases and perpendicular filaments gradually outcompete others because they polymerize the shortest distance to the membrane, where they are protected from capping. This network-intrinsic geometrical adaptation mechanism tunes protrusive force in response to mechanical load."}],"volume":171,"date_created":"2018-12-11T11:48:10Z","language":[{"iso":"eng"}],"publication":"Cell","publication_status":"published","scopus_import":"1","_id":"727"}