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JUN — PLCG2

Text-mined interactions from Literome

Qu et al., Blood 2004 : The antigen induced tyrosine phosphorylation of FcepsilonRI, Syk, phospholipase C-gamma (PLC-gamma) , activation of c-Jun N-terminal kinase (JNK) , extracellular signal regulated kinase ( ERK ), inhibitor of nuclear factor kappaB kinase ( IKK ), and Ca++ influx were all suppressed in the cells overexpressing Cbl-b in the lipid raft
Petlickovski et al., Blood 2005 (Leukemia, Lymphocytic, Chronic, B-Cell...) : This response was characterized by transient phosphorylation of extracellular signal related kinase ( ERK ) and Akt ( protein kinase B [ PKB ] ), lack of activation of c-JUN NH2-terminal kinase (JNK) and p38 mitogen activated protein kinase ( MAPK ), and variable activation of phospholipase Cgamma2 ( PLCgamma2 ) and nuclear factor-kappaB (NF-kappaB)
Yang et al., J Biol Chem 2008 (MAP Kinase Signaling System) : Lastly, we examined the role of the immediate-early transcription factors AP-1 and NF-kappaB and have found that phospholipase C-gamma dependent c-Jun and ERK dependent c-fos, but not the NF-kappaB, are strongly activated by bFGF, which in turn regulates the neuronal differentiation of BMSCs
Chen et al., J Biol Chem 2008 : The lack of PLCgamma2 markedly diminished RANKL induced activation of NF-kappaB, AP-1 , and NFATc1