Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/14140
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dc.titleThe roles of Rac1 and syncollin in regulated exocytosis: Insulin-secreting INS-1 cells as a model
dc.contributor.authorLI JINGSONG
dc.date.accessioned2010-04-08T10:40:15Z
dc.date.available2010-04-08T10:40:15Z
dc.date.issued2004-08-22
dc.identifier.citationLI JINGSONG (2004-08-22). The roles of Rac1 and syncollin in regulated exocytosis: Insulin-secreting INS-1 cells as a model. ScholarBank@NUS Repository.
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/14140
dc.description.abstractRegulated exocytosis, modelled by insulin secretion stimulated by glucose and other secretagogues from pancreatic islet beta cells is mediated by multiple signaling pathways. Rac1, a member of Rho GTPase, primarily regulates the formation of lamellipodial and ruffles by reorganization of cell membrane cortex filamentous actins. By expressing mutated forms of Rac1 in insulin-secreting INS-1 cells that altered the nature of insulin secretion and morphology, this study demonstrated that Rac1 is involved in glucose and forskolin stimulated insulin secretion, probably at the level of recruitment of secretory granules through actin cytoskeletal reorganization. Expression of syncollin, a secretory granule associated protein originally expressed in exocrine cells, in insulin-secreting INS-1 cells, indicated that complete, not truncated form syncollin, can be sorted into insulin secretory granules specifically and impair regulated insulin secretion in a Ca2+-independent way. This suggests that syncollin involve exocytosis in a Ca2+-independent way and possible interacts with SNAREs on distal steps.
dc.language.isoen
dc.subjectExocytosis, Rac1, Syncollin, Insulin secretion, Islet beta-cells, actin cytoskeleton
dc.typeThesis
dc.contributor.departmentNATIONAL UNIVERSITY MEDICAL INSTITUTES
dc.contributor.supervisorLI GUODONG
dc.description.degreePh.D
dc.description.degreeconferredDOCTOR OF PHILOSOPHY
dc.identifier.isiutNOT_IN_WOS
Appears in Collections:Ph.D Theses (Open)

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