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Stimulus–secretion coupling in pancreatic β cells
Author(s) -
Ashcroft Frances M.,
Proks Peter,
Smith Paul A.,
Ämmälä Carina,
Bokvist Krister,
Rorsman Patrik
Publication year - 1994
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240550007
Subject(s) - stimulus (psychology) , secretion , neuroscience , chemistry , biophysics , microbiology and biotechnology , endocrinology , biology , psychology , cognitive psychology
Insulin secretion is triggered by a rise in the intracellular Ca 2+ concentration that results from the activation of voltage‐gated Ca 2+ channels in the β‐cell plasma membrane. Multiple types of β‐cell Ca 2+ channel have been identified in both electrophysiological and molecular biological studies, but it appears that the L‐type Ca 2+ channel plays a dominant role in regulating Ca 2+ 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 Ca 2+ influx, respectively. The mechanism by which elevation of intracellular Ca 2+ leads to the release of insulin granules is not fully understood but appears to involve activation of Ca 2+ /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 β cells. The identification and characterisation of the proteins involved in exocytosis in β cells and clarification of the mechanism(s) of action of Ca 2+ is clearly an important goal for the future. © 1994 Wiley‐Liss, Inc.