Linked Life Data

7929618

Source:http://linkedlifedata.com/resource/pubmed/id/7929618

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1994-10-28
pubmed:abstractText
Insulin secretion is triggered by a rise in the intracellular Ca2+ concentration that results from the activation of voltage-gated Ca2+ channels in the beta-cell plasma membrane. Multiple types of beta-cell Ca2+ channel have been identified in both electrophysiological and molecular biological studies, but it appears that the L-type Ca2+ channel plays a dominant role in regulating Ca2+ influx. Activity of this channel is potentiated by protein kinases A and C and is inhibited by GTP-binding proteins, which may mediate the effects of potentiators and inhibitors of insulin secretion on Ca2+ influx, respectively. The mechanisms by which elevation of intracellular Ca2+ leads to the release of insulin granules is not fully understood but appears to involve activation of Ca2+/calmodulin-dependent protein kinase. Phosphorylation by either protein kinase A or C, probably at different substrates, potentiates insulin secretion by acting at some late stage in the secretory process. There is also evidence that small GTP-binding proteins are involved in regulating exocytosis in beta cells. The identification and characterisation of the proteins involved in exocytosis in beta cells and clarification of the mechanism(s) of action of Ca2+ is clearly an important goal for the future.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0730-2312
pubmed:author
pubmed:issnType
Print
pubmed:volume
55 Suppl
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
54-65
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Stimulus-secretion coupling in pancreatic beta cells.
pubmed:affiliation
University Laboratory of Physiology, Oxford, England.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't