September 2022 "The activation of phospholipase C (PLC) is thought to have a key role in the cardiomyocyte PLC activity results in the generation of diacylglycerol and inositol trisphosphate, which are downstream In this article, we describe the signal transduction elements that regulate PLC gene expression. α1-adrenoceptor signaling pathway and downstream signaling processes that mediate an upregulation of PLC Evidence is also indicated to demonstrate that PLC activities self-regulate the expression of PLC isozymes

Deletion of phospholipase Cβ3 (PLCβ3), or selective inhibition of Gβγ regulation of PLCβ3, enhances the Here we investigated a potential mechanism for regulation of PLC signaling downstream of MOR in HEK293 cells and found that MOR alone could not stimulate PLC, but rather required a coincident signal from These data support a model where Gq and Gβγ-dependent signaling cooperatively regulate PLC activation

signaling through MRGPRD was investigated further by probing downstream signaling effectors along the Gαq/Phospholipase C (PLC) pathway, which results in an IkB kinases (IKK)-mediated canonical activation of nuclear factor could be blocked by a Gαq inhibitor (YM-254890), an IKK complex inhibitor (IKK-16), and partly by a PLC

Abstract " The current dogma is that chemoattractants G protein-coupled receptors (GPCRs) activate β phospholipase C (PLCβ) while receptor tyrosine kinases (RTKs) activate γ phospholipase C (PLCγ). we show that chemoattractant/GPCR-mediated membrane recruitment of PLCγ2 constitutes GPCR-mediated phospholipase C (PLC) signaling and is essential for neutrophil polarization and migration during chemotaxis. C (PLC) , g2 phospholipase C (PLCγ2) .

Finally, we identified that G protein-coupled receptor (GPCR)-phospholipase C (PLC)-inositol trisphosphate G protein-coupled receptor (GPCR)-phospholipase C (PLC)-inositol trisphosphate receptor (IP3R)-SOC signaling

downstream signaling molecules, such as protein kinase A (PKA), phosphatidylinositol 3-kinase (PI3K), and phospholipase C.