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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

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PDGFB — PLCG1

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Sachinidis et al., Br J Pharmacol 2000 : Furthermore CTX attenuated the PDGF-BB induced tyrosine phosphorylation of the PDGF-Rbeta, PI 3'-K, PLC-gamma1 and ERK1/2 indicating an action of cyclic AMP on PDGF-beta receptor
Kim et al., Biochem Pharmacol 2005 : Pre-incubation of rat aortic VSMCs with luteolin significantly inhibited the PDGF-BB induced extracellular signal regulated kinase 1/2 ( ERK1/2 ), Akt and phospholipase C (PLC)-gamma1 activation as well as c-fos gene expression
Kim et al., Arch Pharm Res 2006 : Pre-incubation of the VSMCs with L7G significantly inhibited the PDGF-BB induced extracellular signal regulated kinase 1/2 ( ERK1/2 ), Akt and the phospholipase C (PLC)-gamma1 activation
Kim et al., Biol Pharm Bull 2010 (Cardiovascular Diseases) : In Western blot analysis, PDGF-BB stimulated ( 25 ng/ml ) phospholipase-C (PLC)gamma1 and Akt phosphorylation was inhibited by BST406 ( 0-10microM )
Inui et al., J Biol Chem 1993 : At 37 degrees C, PDGF-AB caused tyrosine phosphorylation of a group of proteins including PDGF-beta receptor and phospholipase C-gamma 1 , but at a slower rate than PDGF-BB
Sachinidis et al., Eur J Cell Biol 1996 : GM2 and GM1 inhibit the PDGF-BB dependent receptor tyrosine autophosphorylation, stimulation of the PLC-gamma 1 , increase of inositol-1,4,5-trisphosphate ( InsP3 ), elevation in cytosolic free Ca2+ ( [ Ca2+ ] i ), expression of the immediate early growth response gene c-fos and cell proliferation with the following rank order of potency GM2 > GM1 ... Although GM3 did not influence the PDGF-BB dependent receptor autophosphorylation and PLC-gamma 1 activation, it effectively inhibited the PDGF-BB dependent InsP3 formation, [ Ca2+ ] i and cell growth ... GM3 was able to suppress the PDGF-BB dependent increase of InsP3 and [ Ca2+ ] i downstream of the PDGF-BB dependent receptor autophosphorylation and PLC-gamma 1 activity