Spatiotemporal Regulators for Insulin-Stimulated GLUT4 Vesicle Exocytosis.

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Insulin 11 endocrinologydiseasesdrugs
diabetes mellitus 1 endocrinologydiseases
hyperinsulinemia 1 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 65 Title: Journal of Diabetes ResearchSpatiotemporal Regulators for Insulin -Stimulated GLUT4 Vesicle ExocytosisXiaoxu ZhouPing ShentuYingke XuDepartment of Biomedical Engineering,
Insulin 480 University, Hangzhou 310027, ChinaPublication date (ppub): /2017Publication date (epub): 4/2017Abstract Insulin increases glucose uptake and storage in muscle and adipose cells, which is accomplished through the
Insulin 2261 5–10% of the GLUT4 is located at the cell surface and >90% in intracellular membrane compartments. Insulin stimulation shifts the steady-state distribution of GLUT4 towards the plasma membrane. The dysfunction
Insulin 2983 coupling between the signaling and intracellular vesicle trafficking is still not fully understood. Insulin regulates GLUT4 vesicle exocytosis in a temporal and spatial manner. Insulin initiates rapid signaling
Insulin 3060 not fully understood. Insulin regulates GLUT4 vesicle exocytosis in a temporal and spatial manner. Insulin initiates rapid signaling transduction cascades that propagate into the cell to mobilize GLUT4 vesicle
Insulin 3635 proteins are involved in spatiotemporal regulation of GLUT4 vesicle exocytosis.2. Temporal Regulators of Insulin -Stimulated GLUT4 TranslocationInsulin stimulates the surface accumulation of GLUT4 with a half time
Insulin 3673 regulation of GLUT4 vesicle exocytosis.2. Temporal Regulators of Insulin-Stimulated GLUT4 Translocation Insulin stimulates the surface accumulation of GLUT4 with a half time of 2–5 minutes, which reaches a plateau
Insulin 4032 and trafficking [[9]], vesicle tethering/docking [[10]–[12]], and ultimately fusion [[13]–[15]]. Insulin signaling is initiated through binding and activation of its surface receptor. Activation of the insulin
Insulin 8199 [[38], [39]]. AS160 is a Rab GTPase-activating protein (Rab-GAP), which is present on GLUT4 vesicles. Insulin causes the phosphorylation of AS160 at multiple serine/threonine residues, which inactivate its GAP
Insulin 13831 and can also regulate the interaction between Rab4 and kinesin motors [[72], [73]].2.5. Rac and TC10 Insulin -stimulated GLUT4 translocation requires dynamic changes in the actin cytoskeleton or called actin remodeling.
Insulin 17416 effectors of TC10 regulate discrete steps of GLUT4 trafficking in cells.3. Spatial Determinants of Insulin -Regulated GLUT4 TranslocationThe spatial aspects of insulin signal transduction and distribution of
Select Disease Character Offset Disease Term Instance
diabetes mellitus 2491 insulin-stimulated GLUT4 translocation is highly related to peripheral insulin resistance and non-insulin-dependent diabetes mellitus in human beings [[2]].Multiple insulin signaling pathways have been implicated in GLUT4 regulation,
hyperinsulinemia 1811 of the GLUT4 gene specifically in mice muscle or adipose tissues results in impaired glucose uptake, hyperinsulinemia , and peripheral insulin resistance [[4], [5]]. The major physiological action of insulin is to increase

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