2014
DOI: 10.1007/s12013-014-9992-6
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Regulation of Gβγi-Dependent PLC-β3 Activity in Smooth Muscle: Inhibitory Phosphorylation of PLC-β3 by PKA and PKG and Stimulatory Phosphorylation of Gαi-GTPase-Activating Protein RGS2 by PKG

Abstract: In gastrointestinal smooth muscle, agonists that bind to Gi-coupled receptors activate preferentially PLC-β3 via Gβγ to stimulate phosphoinositide (PI) hydrolysis and generate inositol 1,4,5-trisphosphate (IP3) leading to IP3-dependent Ca2+ release and muscle contraction. In the present study, we identified the mechanism of inhibition of PLC-β3-dependent PI hydrolysis by cAMP-dependent protein kinase (PKA) and cGMP-dependent protein kinase (PKG). Cyclopentyl adenosine (CPA), an adenosine A1 receptor agonist ca… Show more

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Cited by 30 publications
(24 citation statements)
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“…Thus, it is possible that vasodilators that act through the cAMP-PKA signaling cascade, could act, in part, by inhibition of IP 3 R function in vascular SMCs. Increased cAMP-PKA activity also can inhibit the production of IP 3 via inhibition of PLCs (4, 1051). This would indirectly inhibit Ca 2+ release through IP 3 Rs.…”
Section: Inositol-145-triphosphate Receptorsmentioning
confidence: 99%
See 1 more Smart Citation
“…Thus, it is possible that vasodilators that act through the cAMP-PKA signaling cascade, could act, in part, by inhibition of IP 3 R function in vascular SMCs. Increased cAMP-PKA activity also can inhibit the production of IP 3 via inhibition of PLCs (4, 1051). This would indirectly inhibit Ca 2+ release through IP 3 Rs.…”
Section: Inositol-145-triphosphate Receptorsmentioning
confidence: 99%
“…10). The cGMP-PKG signaling pathway also can inhibit formation of IP 3 via PLCs to inhibit Ca 2+ release through IP 3 Rs (4, 1051). …”
Section: Inositol-145-triphosphate Receptorsmentioning
confidence: 99%
“…Feedback Control of Second Messengers Signaling Systems in White Adipose Tissue Adipocytes… http://dx.doi.org/10.5772/intechopen.75703 2.2.1. Ca 2+ /phospholipase C/IP3/IP3R/Ca 2+ positive feedback signaling systemNumerous external signals, by stimulating Gq proteins and tyrosine kinase (TK) coupled receptors, result in the formation of IP3 by various isoforms of phospholipase C (PLC)[24,25,38] with subsequent activation of IP3R-channels and rise of Ca 2+ in the cytoplasm via CICR mechanism:…”
mentioning
confidence: 99%
“…Inhibition of phosphoinositide (PI) hydrolysis in smooth muscles is done via phosphorylation of RGS2 by PRKG and its association with Gα-GTP subunit of G proteins. In fact, PRKG over-activates RGS2 to accelerate Gα-GTPase activity and enhance Gαβγ (complete G protein) trimer formation (56). Consequently, there would be a possibility that Src can induce RGS2 protein activity regarding the edge information in pathway 7.…”
Section: Discussionmentioning
confidence: 99%