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10.1038/ncomms6974 http://scihub22266oqcxt.onion/10.1038/ncomms6974 C4353700!4353700!25569184     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2015 ; 6 (ä): 5974 Nephropedia Template TP {{tp|p=25569184|t=2015. Membrane tension and peripheral protein density mediate membrane shape transitions |pdf=|usr=}}{{25569184}} gab.com Text Membrane tension and peripheral protein density mediate membrane shape transitions JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25569184 #FOAvip Endocytosis is a ubiquitous eukaryotic membrane budding, vesiculation, and internalization process fulfilling numerous roles including compensation of membrane area increase after bursts of exocytosis. The mechanism of the coupling between these two processes to enable homeostasis is not well understood. Recently, an ultrafast endocytosis (UFE) pathway was revealed with a speed significantly exceeding classical clathrin-mediated endocytosis (CME). Membrane tension reduction is a potential mechanism by which endocytosis can be rapidly activated at remote sites. Here we provide experimental evidence for a mechanism whereby membrane tension reduction initiates membrane budding and tubulation mediated by endocytic proteins such as endophilin A1. We find that shape instabilities occur at well-defined membrane tensions and surface densities of endophilin. From our data, we obtain a membrane shape stability diagram that shows remarkable consistency with a quantitative model. This model applies to all laterally diffusive curvature coupling proteins and therefore a wide range of endocytic proteins. Twit Text FOAVip Membrane tension and peripheral protein density mediate membrane shape transitions ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=25569184 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25569184 #FOAvip English Wikipedia <ref>{{Cite pmid|25569184}}</ref> Membrane tension and peripheral protein density mediate membrane shape transitions #MMPMID25569184 Shi Z; Baumgart T Nat Commun 2015[]; 6 (ä): 5974 PMID25569184show ga Endocytosis is a ubiquitous eukaryotic membrane budding, vesiculation, and internalization process fulfilling numerous roles including compensation of membrane area increase after bursts of exocytosis. The mechanism of the coupling between these two processes to enable homeostasis is not well understood. Recently, an ultrafast endocytosis (UFE) pathway was revealed with a speed significantly exceeding classical clathrin-mediated endocytosis (CME). Membrane tension reduction is a potential mechanism by which endocytosis can be rapidly activated at remote sites. Here we provide experimental evidence for a mechanism whereby membrane tension reduction initiates membrane budding and tubulation mediated by endocytic proteins such as endophilin A1. We find that shape instabilities occur at well-defined membrane tensions and surface densities of endophilin. From our data, we obtain a membrane shape stability diagram that shows remarkable consistency with a quantitative model. This model applies to all laterally diffusive curvature coupling proteins and therefore a wide range of endocytic proteins. äMembrane tension and peripheral protein density mediate membrane shape(epmc).pdf DeepDyve Pubget Overpricing