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10.1083/jcb.201704061 http://scihub22266oqcxt.onion/10.1083/jcb.201704061 C5674896!5674896 !28923975     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28923975 &cmd=llinks): Failed to open stream: HTTP request failed! 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Control of actin polymerization via the coincidence of phosphoinositides and high membrane curvature |pdf=|usr=}}{{28923975 }} gab.com Text Control of actin polymerization via the coincidence of phosphoinositides and high membrane curvature JO: J Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=28923975 #FOAvip The conditional use of actin during clathrin-mediated endocytosis in mammalian cells suggests that the cell controls whether and how actin is used. Using a combination of biochemical reconstitution and mammalian cell culture, we elucidate a mechanism by which the coincidence of PI(4,5)P(2) and PI(3)P in a curved vesicle triggers actin polymerization. At clathrin-coated pits, PI(3)P is produced by the INPP4A hydrolysis of PI(3,4)P(2), and this is necessary for actin-driven endocytosis. Both Cdc42?guanosine triphosphate and SNX9 activate N-WASP-WIP- and Arp2/3-mediated actin nucleation. Membrane curvature, PI(4,5)P(2), and PI(3)P signals are needed for SNX9 assembly via its PX-BAR domain, whereas signaling through Cdc42 is activated by PI(4,5)P(2) alone. INPP4A activity is stimulated by high membrane curvature and synergizes with SNX9 BAR domain binding in a process we call curvature cascade amplification. We show that the SNX9-driven actin comets that arise on human disease-associated oculocerebrorenal syndrome of Lowe (OCRL) deficiencies are reduced by inhibiting PI(3)P production, suggesting PI(3)P kinase inhibitors as a therapeutic strategy in Lowe syndrome. Twit Text FOAVip Control of actin polymerization via the coincidence of phosphoinositides and high membrane curvature ????J Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=28923975 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28923975 #FOAvip English Wikipedia <ref>{{Cite pmid|28923975 }}</ref> Control of actin polymerization via the coincidence of phosphoinositides and high membrane curvature #MMPMID28923975 Daste F ; Walrant A ; Holst MR ; Gadsby JR ; Mason J ; Lee JE ; Brook D ; Mettlen M ; Larsson E ; Lee SF ; Lundmark R ; Gallop JL J Cell Biol 2017[Nov]; 216 (11 ): 3745-3765 PMID28923975 show ga The conditional use of actin during clathrin-mediated endocytosis in mammalian cells suggests that the cell controls whether and how actin is used. Using a combination of biochemical reconstitution and mammalian cell culture, we elucidate a mechanism by which the coincidence of PI(4,5)P(2) and PI(3)P in a curved vesicle triggers actin polymerization. At clathrin-coated pits, PI(3)P is produced by the INPP4A hydrolysis of PI(3,4)P(2), and this is necessary for actin-driven endocytosis. Both Cdc42?guanosine triphosphate and SNX9 activate N-WASP-WIP- and Arp2/3-mediated actin nucleation. Membrane curvature, PI(4,5)P(2), and PI(3)P signals are needed for SNX9 assembly via its PX-BAR domain, whereas signaling through Cdc42 is activated by PI(4,5)P(2) alone. INPP4A activity is stimulated by high membrane curvature and synergizes with SNX9 BAR domain binding in a process we call curvature cascade amplification. We show that the SNX9-driven actin comets that arise on human disease-associated oculocerebrorenal syndrome of Lowe (OCRL) deficiencies are reduced by inhibiting PI(3)P production, suggesting PI(3)P kinase inhibitors as a therapeutic strategy in Lowe syndrome. |*Endocytosis [MESH] |Actin-Related Protein 2-3 Complex/genetics/metabolism [MESH] |Actins/*metabolism [MESH] |Animals [MESH] |CRISPR-Cas Systems [MESH] |Clathrin-Coated Vesicles/*metabolism [MESH] |Clathrin/*metabolism [MESH] |Coated Pits, Cell-Membrane/*metabolism [MESH] |Cytoskeletal Proteins/genetics/metabolism [MESH] |HeLa Cells [MESH] |Humans [MESH] |Hydrolysis [MESH] |Intracellular Signaling Peptides and Proteins/genetics/metabolism [MESH] |Oculocerebrorenal Syndrome/genetics/metabolism [MESH] |Phosphatidylinositol 4,5-Diphosphate/metabolism [MESH] |Phosphatidylinositol Phosphates/metabolism [MESH] |Phosphatidylinositols/*metabolism [MESH] |Phosphoric Monoester Hydrolases/genetics/metabolism [MESH] |Protein Multimerization [MESH] |RNA Interference [MESH] |Retinal Pigment Epithelium/metabolism [MESH] |Signal Transduction [MESH] |Sorting Nexins/genetics/metabolism [MESH] |Time Factors [MESH] |Transfection [MESH] |Wiskott-Aldrich Syndrome Protein, Neuronal/genetics/metabolism [MESH] |Xenopus laevis [MESH]Control of actin polymerization via the coincidence of phosphoinositid(epmc).pdf DeepDyve Pubget Overpricing