TY - JOUR
T1 - Regulation of CaV2 calcium channels by G protein coupled receptors
AU - Zamponi, Gerald W.
AU - Currie, Kevin P.M.
N1 - Funding Information:
Work in the Currie lab is supported by the National Institutes of Health, National Institute of Neurological Disorders And Stroke [Grant R01-NS052446 ], and by the American Heart Association. GWZ is supported by the Canadian Institutes of Health Research , is an AI-HS Scientist and a Canada Research Chair. The molecular graphics images in Fig. 3 were produced using the UCSF Chimera package from the Resource for Biocomputing, Visualization, and Informatics at the University of California, San Francisco (supported by NIH P41 RR001081) [256,257] .
PY - 2013/7
Y1 - 2013/7
N2 - Voltage gated calcium channels (Ca2 + channels) are key mediators of depolarization induced calcium influx into excitable cells, and thereby play pivotal roles in a wide array of physiological responses. This review focuses on the inhibition of CaV2 (N- and P/Q-type) Ca 2 +-channels by G protein coupled receptors (GPCRs), which exerts important autocrine/paracrine control over synaptic transmission and neuroendocrine secretion. Voltage-dependent inhibition is the most widespread mechanism, and involves direct binding of the G protein βγ dimer (Gβγ) to the α1 subunit of CaV2 channels. GPCRs can also recruit several other distinct mechanisms including phosphorylation, lipid signaling pathways, and channel trafficking that result in voltage-independent inhibition. Current knowledge of Gβγ-mediated inhibition is reviewed, including the molecular interactions involved, determinants of voltage-dependence, and crosstalk with other cell signaling pathways. A summary of recent developments in understanding the voltage-independent mechanisms prominent in sympathetic and sensory neurons is also included. This article is part of a Special Issue entitled: Calcium channels.
AB - Voltage gated calcium channels (Ca2 + channels) are key mediators of depolarization induced calcium influx into excitable cells, and thereby play pivotal roles in a wide array of physiological responses. This review focuses on the inhibition of CaV2 (N- and P/Q-type) Ca 2 +-channels by G protein coupled receptors (GPCRs), which exerts important autocrine/paracrine control over synaptic transmission and neuroendocrine secretion. Voltage-dependent inhibition is the most widespread mechanism, and involves direct binding of the G protein βγ dimer (Gβγ) to the α1 subunit of CaV2 channels. GPCRs can also recruit several other distinct mechanisms including phosphorylation, lipid signaling pathways, and channel trafficking that result in voltage-independent inhibition. Current knowledge of Gβγ-mediated inhibition is reviewed, including the molecular interactions involved, determinants of voltage-dependence, and crosstalk with other cell signaling pathways. A summary of recent developments in understanding the voltage-independent mechanisms prominent in sympathetic and sensory neurons is also included. This article is part of a Special Issue entitled: Calcium channels.
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U2 - 10.1016/j.bbamem.2012.10.004
DO - 10.1016/j.bbamem.2012.10.004
M3 - Review article
C2 - 23063655
AN - SCOPUS:84876919334
VL - 1828
SP - 1629
EP - 1643
JO - Biochimica et Biophysica Acta - Biomembranes
JF - Biochimica et Biophysica Acta - Biomembranes
SN - 0005-2736
IS - 7
ER -