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From Proteopedia
Crystal Structure of the Sec13-Sec16 blade-inserted complex from Pichia pastoris
Structural highlights
FunctionQ45TY0_PICPA SEC13_KOMPG Component of the coat protein complex II (COPII) which promotes the formation of transport vesicles from the endoplasmic reticulum (ER). The coat has two main functions, the physical deformation of the endoplasmic reticulum membrane into vesicles and the selection of cargo molecules. It also functions as a component of the nuclear pore complex (NPC). NPC components, collectively referred to as nucleoporins (NUPs), can play the role of both NPC structural components and of docking or interaction partners for transiently associated nuclear transport factors. SEC13 is required for efficient mRNA export from the nucleus to the cytoplasm and for correct nuclear pore biogenesis and distribution (By similarity).[UniProtKB:Q04491] Publication Abstract from PubMedDuring the budding of COPII vesicles from transitional ER (tER) sites, Sec16 has been proposed to play two distinct roles: negatively regulating COPII turnover, and organizing COPII assembly at tER sites. We tested these ideas using the yeast Pichia pastoris. Redistribution of Sec16 to the cytosol accelerates tER dynamics, supporting a negative regulatory role for Sec16. To evaluate a possible COPII organization role, we dissected the functional regions of Sec16. The central conserved domain (CCD), which had been implicated in coordinating COPII assembly, is actually dispensable for normal tER structure. An upstream conserved region (UCR) localizes Sec16 to tER sites. The UCR binds COPII components, and removal of COPII from tER sites also removes Sec16, indicating that COPII recruits Sec16 rather than the other way around. We propose that Sec16 does not in fact organize COPII. Instead, regulation of COPII turnover can account for the influence of Sec16 on tER sites. Sec16 influences transitional ER sites by regulating rather than organizing COPII.,Bharucha N, Liu Y, Papanikou E, McMahon C, Esaki M, Jeffrey PD, Hughson FM, Glick BS Mol Biol Cell. 2013 Sep 4. PMID:24006484[1] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. References
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