جهت دسترسی به کاربرگه ی زیر، از این لینک استفاده کنید. http://dl.pgu.ac.ir/handle/Hannan/63865
Title: OCRL1 engages with the F-BAR protein pacsin 2 to promote biogenesis of membrane-trafficking intermediates
Keywords: Science & Technology;Life Sciences & Biomedicine;Cell Biology;TRANS-GOLGI NETWORK;MEDIATES RETROGRADE TRANSPORT;MANNOSE 6-PHOSPHATE RECEPTOR;LOWE-SYNDROME;OCULOCEREBRORENAL SYNDROME;SUBCELLULAR-LOCALIZATION;PHYSIOLOGICAL FUNCTIONS;ENDOCYTIC PROTEINS;CELL REGULATION;ACTIN DYNAMICS;Developmental Biology;06 Biological Sciences;11 Medical And Health Sciences
Issue Date: 24-Aug-2016
Publisher: American Society for Cell Biology
Description: Mutation of the inositol 5-phosphatase OCRL1 causes Lowe syndrome and Dent-2 disease. Loss of OCRL1 function perturbs several cellular processes, including membrane traffic, but the underlying mechanisms remain poorly defined. Here we show that OCRL1 is part of the membrane-trafficking machinery operating at the trans-Golgi network (TGN)/endosome interface. OCRL1 interacts via IPIP27A with the F-BAR protein pacsin 2. OCRL1 and IPIP27A localize to mannose 6-phosphate receptor (MPR)–containing trafficking intermediates, and loss of either protein leads to defective MPR carrier biogenesis at the TGN and endosomes. OCRL1 5-phosphatase activity, which is membrane curvature sensitive, is stimulated by IPIP27A-mediated engagement of OCRL1 with pacsin 2 and promotes scission of MPR-containing carriers. Our data indicate a role for OCRL1, via IPIP27A, in regulating the formation of pacsin 2–dependent trafficking intermediates and reveal a mechanism for coupling PtdIns(4,5)P2 hydrolysis with carrier biogenesis on endomembranes.
URI: https://dx.doi.org/10.1091/mbc.E15-06-0329
Other Identifiers: 1939-4586
http://hdl.handle.net/10044/1/39416
EP/K039946/1
IC/ICAP/2012
Type Of Material: OTHER
Appears in Collections:Chemistry

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