Glucose stimulation of insulin release in the absence of extracellular Ca2+ and in the absence of any increase in intracellular Ca2+ in rat pancreatic islets.
about
Glucagon-like peptide-1 mobilizes intracellular Ca2+ and stimulates mitochondrial ATP synthesis in pancreatic MIN6 beta-cellsNutrient-stimulated insulin secretion in mouse islets is critically dependent on intracellular pHcAMP-dependent mobilization of intracellular Ca2+ stores by activation of ryanodine receptors in pancreatic beta-cells. A Ca2+ signaling system stimulated by the insulinotropic hormone glucagon-like peptide-1-(7-37)Protein acylation in the inhibition of insulin secretion by norepinephrine, somatostatin, galanin, and PGE2.Mechanisms of inhibition of insulin release.Lacritin-induced secretion of tear proteins from cultured monkey lacrimal acinar cellsCaV2.3 channel and PKClambda: new players in insulin secretionStimulation of exocytosis without a calcium signal.MafA is a key regulator of glucose-stimulated insulin secretion.Contribution of protein kinase Cα in the stimulation of insulin by the down-regulation of Cavβ subunits.One process for pancreatic beta-cell coalescence into islets involves an epithelial-mesenchymal transition.Hypothesis: one rate-limiting step controls the magnitude of both phases of glucose-stimulated insulin secretion.GPCR mediated regulation of synaptic transmission.Dopamine synthesis and D3 receptor activation in pancreatic β-cells regulates insulin secretion and intracellular [Ca(2+)] oscillations.Defective insulin secretion and enhanced insulin action in KATP channel-deficient mice.Cell swelling-induced peptide hormone secretion.Minireview: intraislet regulation of insulin secretion in humans.Glucose-stimulated insulin secretion: A newer perspective.Activation of the KATP channel-independent signaling pathway by the nonhydrolyzable analog of leucine, BCH.Noradrenaline inhibits exocytosis via the G protein βγ subunit and refilling of the readily releasable granule pool via the α(i1/2) subunit.Overexpression of a modified human malonyl-CoA decarboxylase blocks the glucose-induced increase in malonyl-CoA level but has no impact on insulin secretion in INS-1-derived (832/13) beta-cells.An endogenous peptide isolated from the gut, NK-lysin, stimulates insulin secretion without changes in cytosolic free Ca2+ concentration.Rapid activation and nuclear translocation of mitogen-activated protein kinases in response to physiological concentration of glucose in the MIN6 pancreatic beta cell line.Augmentation of basal insulin release from rat islets by preexposure to a high concentration of glucose.Anaplerotic input is sufficient to induce time-dependent potentiation of insulin release in rat pancreatic islets.
P2860
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P2860
Glucose stimulation of insulin release in the absence of extracellular Ca2+ and in the absence of any increase in intracellular Ca2+ in rat pancreatic islets.
description
1995 nî lūn-bûn
@nan
1995 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
1995 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
1995年の論文
@ja
1995年論文
@yue
1995年論文
@zh-hant
1995年論文
@zh-hk
1995年論文
@zh-mo
1995年論文
@zh-tw
1995年论文
@wuu
name
Glucose stimulation of insulin ...... Ca2+ in rat pancreatic islets.
@ast
Glucose stimulation of insulin ...... Ca2+ in rat pancreatic islets.
@en
type
label
Glucose stimulation of insulin ...... Ca2+ in rat pancreatic islets.
@ast
Glucose stimulation of insulin ...... Ca2+ in rat pancreatic islets.
@en
prefLabel
Glucose stimulation of insulin ...... Ca2+ in rat pancreatic islets.
@ast
Glucose stimulation of insulin ...... Ca2+ in rat pancreatic islets.
@en
P2093
P2860
P356
P1476
Glucose stimulation of insulin ...... Ca2+ in rat pancreatic islets
@en
P2093
P2860
P304
10728-10732
P356
10.1073/PNAS.92.23.10728
P407
P577
1995-11-01T00:00:00Z