Receptor-operated calcium influx mediated by protein tyrosine kinase pathways.
Calcium influx from the extracellular space elicited by activation of heterotrimeric G protein-coupled and heptahelical receptors plays a critical role in transmembrane signal transduction in a wide variety of cell systems. In nonexcitable cells, the precise voltage-independent mechanism by which calcium enters the cell remains unknown. Multiple mechanisms appear to be operating in different cell types (1-3): 1. G protein-operated calcium influx, 2. Second messenger-operated calcium influx, 3. Capacitative calcium influx, and 4. Phosphorylation of calcium channels. Receptor-operated calcium channels have a fundamental role in stimulus-secretion coupling in many different cells, but these channels remain to be purified and cloned. This review proposes that receptor-operated calcium influx is mediated by protein tyrosine kinase pathways. The function of protein tyrosine kinase pathways and their interactions with other receptor-operated calcium influx mechanisms are described.
Tsunoda
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Y
Department of Internal Medicine, University of Michigan, Ann Arbor 48109-0682, USA.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D000242:Cyclic AMP / Q000502:physiology; D006152:Cyclic GMP / Q000502:physiology; D019204:GTP-Binding Proteins / Q000502:physiology; D019833:Genistein / Q000494:pharmacology; D006801:Humans; D007295:Inositol Phosphates / Q000502:physiology; D010766:Phosphorylation; D011505:Protein-Tyrosine Kinases / Q000502:physiology*; D011956:Receptors, Cell Surface / Q000502:physiology*
D015220:Calcium Channels; D007295:Inositol Phosphates; D011956:Receptors, Cell Surface; D019833:Genistein; D000242:Cyclic AMP; D011505:Protein-Tyrosine Kinases; D019204:GTP-Binding Proteins; D006152:Cyclic GMP; D002118:Calcium