PLCG1 disassociates from VEGFR2 and translocate to PM

Following tyrosine phosphorylation and activation, PLCG1 dissociates from the VEGFR2 receptor and associates with its substrate phosphatidylinositol (4,5)-bisphosphate (PIP2) in the plasma membrane. PLCG1 hydrolyses PIP2 resulting in the generation of diacylglycerol (DAG) and inositol 1,4,5-trisphosphate (IP3). DAG is an activator of PKC which leads to subsequent activation of MAP kinase, resulting in increased endothelial cell proliferation. IP3 acts upon receptors in the endoplasmic reticulum causing release of intracellular calcium. Elevation of cytosolic Ca2+ stimulates eNOS to produce nitric oxide (NO) causing vascular dilation. Entry of extracellular calcium through specific channels is important for the activation of certain proteins (Takahashi et al. 2001, Takahashi et al. 1999, Xia et al. 1996).

在酪氨酸磷酸化和激活之后，PLC G1蛋白从VEGFR2受体上解离，并在质膜上与底物磷脂酰肌醇(4,5)-二磷酸(PIP2)结合。PLC G1蛋白水解PIP2，进而生成二酰甘油(DAG)和肌醇1,4,5-三磷酸(IP3)。DAG作为PKC的激活剂，进而引发MAP激酶的激活，导致内皮细胞的增殖增加。IP3作用于内质网上的受体，引起细胞内钙离子的释放。细胞质中钙离子浓度的升高刺激eNOS产生一氧化氮(NO)，导致血管舒张。通过特定通道进入的细胞外钙离子对于某些蛋白质的激活至关重要（Takahashi等，2001年，Takahashi等，1999年，Xia等，1996年）。