A highly Ca2+-sensitive pool of granules is regulated by glucose and protein kinases in insulin-secreting INS-1 cells
about
Mechanisms of action of glucagon-like peptide 1 in the pancreasCyclic AMP dynamics in the pancreatic β-cellInsulin secretion: a high-affinity Ca2+ sensor after all?Unifying concepts in stimulus-secretion coupling in endocrine cells and some implications for therapeutics.Distinct actions of Rab3 and Rab27 GTPases on late stages of exocytosis of insulin.Ca2+ channel clustering with insulin-containing granules is disturbed in type 2 diabetesPKA-dependent potentiation of glucose-stimulated insulin secretion by Epac activator 8-pCPT-2'-O-Me-cAMP-AM in human islets of Langerhans.Cyclic AMP potentiates Ca2+-dependent exocytosis in pancreatic duct epithelial cells.Lessons from models of pancreatic beta cells for engineering glucose-sensing cellsActivators of PKA and Epac distinctly influence insulin secretion and cytosolic Ca2+ in female mouse islets stimulated by glucose and tolbutamide.Phospholipase C-ε links Epac2 activation to the potentiation of glucose-stimulated insulin secretion from mouse islets of LangerhansMunc18-1 and Munc18-2 proteins modulate beta-cell Ca2+ sensitivity and kinetics of insulin exocytosis differently.Calcium current inactivation rather than pool depletion explains reduced exocytotic rate with prolonged stimulation in insulin-secreting INS-1 832/13 cells.The isolated pancreatic islet as a micro-organ and its transplantation to cure diabetes: celebrating the legacy of Paul Lacy.Evolving insights regarding mechanisms for the inhibition of insulin release by norepinephrine and heterotrimeric G proteins.Phosphomimetic mutation of Ser-187 of SNAP-25 increases both syntaxin binding and highly Ca2+-sensitive exocytosis.Glucose-sensing mechanisms in pancreatic beta-cells.PKC-induced sensitization of Ca2+-dependent exocytosis is mediated by reducing the Ca2+ cooperativity in pituitary gonadotropes.Protein kinase activation increases insulin secretion by sensitizing the secretory machinery to Ca2+.Insulin vesicle release: walk, kiss, pause ... then run.Identifying the targets of the amplifying pathway for insulin secretion in pancreatic beta-cells by kinetic modeling of granule exocytosis.Novel aspects of the molecular mechanisms controlling insulin secretion.Newcomer insulin secretory granules as a highly calcium-sensitive poolContributions of mathematical modeling of beta cells to the understanding of beta-cell oscillations and insulin secretionMolecular physiology of glucagon-like peptide-1 insulin secretagogue action in pancreatic β cells.Modes of exocytosis and electrogenesis underlying canine biphasic insulin secretion.On depolarization-evoked exocytosis as a function of calcium entry: possibilities and pitfalls.Neurosecretion: what can we learn from chromaffin cells.Pig-to-Primate Islet Xenotransplantation: Past, Present, and Future.Progress in Clinical Encapsulated Islet Xenotransplantation.Free Fatty Acid Receptor 1 (FFAR1) as an Emerging Therapeutic Target for Type 2 Diabetes Mellitus: Recent Progress and Prevailing Challenges.Noradrenaline inhibits exocytosis via the G protein βγ subunit and refilling of the readily releasable granule pool via the α(i1/2) subunit.ARA290 improves insulin release and glucose tolerance in type 2 diabetic GK rats.Enhanced Rap1 activation and insulin secretagogue properties of an acetoxymethyl ester of an Epac-selective cyclic AMP analog in rat INS-1 cells: studies with 8-pCPT-2'-O-Me-cAMP-AM.Cell-permeable peptide-based disruption of endogenous PKA-AKAP complexes: a tool for studying the molecular roles of AKAP-mediated PKA subcellular anchoring.Controlled on-chip stimulation of quantal catecholamine release from chromaffin cells using photolysis of caged Ca2+ on transparent indium-tin-oxide microchip electrodes.Short-term potentiation of membrane resealing in neighboring cells is mediated by purinergic signaling.Glucose-dependent potentiation of mouse islet insulin secretion by Epac activator 8-pCPT-2'-O-Me-cAMP-AM.Alpha-latrotoxin induces exocytosis by inhibition of voltage-dependent K+ channels and by stimulation of L-type Ca2+ channels via latrophilin in beta-cells.Mathematical modeling of insulin secretion and the role of glucose-dependent mobilization, docking, priming and fusion of insulin granules.
P2860
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P2860
A highly Ca2+-sensitive pool of granules is regulated by glucose and protein kinases in insulin-secreting INS-1 cells
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年学术文章
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2004年学术文章
@zh-cn
2004年学术文章
@zh-hans
2004年学术文章
@zh-my
2004年学术文章
@zh-sg
2004年學術文章
@yue
2004年學術文章
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name
A highly Ca2+-sensitive pool o ...... insulin-secreting INS-1 cells
@ast
A highly Ca2+-sensitive pool o ...... insulin-secreting INS-1 cells
@en
type
label
A highly Ca2+-sensitive pool o ...... insulin-secreting INS-1 cells
@ast
A highly Ca2+-sensitive pool o ...... insulin-secreting INS-1 cells
@en
prefLabel
A highly Ca2+-sensitive pool o ...... insulin-secreting INS-1 cells
@ast
A highly Ca2+-sensitive pool o ...... insulin-secreting INS-1 cells
@en
P2860
P356
P1476
A highly Ca2+-sensitive pool o ...... insulin-secreting INS-1 cells
@en
P2093
Kevin D Gillis
P2860
P304
P356
10.1085/JGP.200409081
P577
2004-12-01T00:00:00Z