- ►nih.gov H Kanda, Y Tamori, H Shinoda, M … - Journal of Clinical …, 2005 - Am Soc Clin Investig Insulin-stimulated glucose uptake in adipocytes is mediated by translocation of vesicles containing
the glucose transporter GLUT4 from intracellular storage sites to the cell periphery and the
subsequent fusion of these vesicles ... Cited by 76 - Related articles - All 12 versions
- ►diabetesjournals.org JE Ayala, DP Bracy, OP McGuinness, DH Wasserman - Diabetes, 2006 - Am Diabetes Assoc Despite increased use of the hyperinsulinemic-euglycemic clamp to study insulin action in mice, the
effects of experimental parameters on the results obtained have not been addressed. In our studies,
we determined the influences of ... Cited by 42 - Related articles - BL Direct - All 7 versions
E Oh, BA Spurlin, JE Pessin, DC Thurmond - Diabetes, 2005 - Am Diabetes Assoc The disruption of Munc18c binding to syntaxin 4 impairs insulin-stimulated GLUT4 vesicle
translocation in 3T3L1 adipocytes. To investigate the physiological function and requirement for
Munc18c in the regulation of GLUT4 ... Cited by 34 - Related articles - All 6 versions
CP Hodgkinson, A Mander, GJ Sale - Biochemical Journal, 2005 - pubmedcentral.nih.gov PKCζ (protein kinase Cζ) is a serine/threonine protein kinase controlled by insulin, various
growth factors and phosphoinositide 3-kinase. It has been implicated in controlling glucose
transport in response to insulin by ... Cited by 23 - Related articles - All 10 versions
- ►jbc.org E Oh, DC Thurmond - Journal of Biological Chemistry, 2006 - ASBMB Stimulus-induced tyrosine phosphorylation of Munc18c was investigated as a potential regulatory
mechanism by which the Munc18c-Syntaxin 4 complex can be dissociated in response to divergent
stimuli in multiple cell types. Use ... Cited by 21 - Related articles - BL Direct - All 6 versions
- ►endojournals.org BA Spurlin, DC Thurmond - Molecular Endocrinology, 2006 - Endocrine Soc Numerous overexpression studies have recently implicated Syntaxin 4 as an effector of insulin
secretion, although its requirement in insulin granule exocytosis is unknown. To address this,
islets from Syntaxin 4 heterozygous ... Cited by 22 - Related articles - BL Direct - All 4 versions
CP Hodgkinson, A Mander, GJ Sale - Diabetologia, 2005 - Springer Abstract Aims/hypothesis: Insulin-stimulated glucose transport requires a signalling cascade through
kinases protein kinase (PK) Cζ/λ and PKB that leads to movement of GLUT4 vesicles to the plasma
membrane. The aim of this study was ... Cited by 19 - Related articles - BL Direct - All 5 versions
- ►diabetesjournals.org BA Spurlin, SY Park, AK Nevins, JK Kim, DC Thurmond - Diabetes, 2004 - Am Diabetes Assoc Insulin-stimulated translocation of GLUT4 vesicles from an intracellular compartment to the plasma
membrane in 3T3L1 adipocytes is mediated through a syntaxin 4 (Syn4)- and Munc18c-dependent
mechanism. To investigate the ... Cited by 19 - Related articles - BL Direct - All 5 versions
Z Wang, E Oh, DC Thurmond - Journal of Biological Chemistry, 2007 - ASBMB The small Rho family GTPases Cdc42 and Rac1 have each been shown to function in insulin exocytosis
and are presumed to function in actin remodeling and insulin granule mobilization. However, whether
either GTPase is required for the ... Cited by 14 - Related articles - All 6 versions
HY Gaisano, L Sheu, D Whitcomb - Pancreas, 2004 - journals.lww.com Abstract: The minimal machinery for fusion of secretory vesicles with the cell membrane is a cognate
set of v- and t-SNAREs on op- posing membranes. Spontaneous SNARE complex assembly leading to
unregulated membrane fusion is ... Cited by 12 - Related articles - BL Direct - All 3 versions
