Gene interactions and pathways from curated databases and text-mining

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PDGFB — STAT3

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Neeli et al., J Biol Chem 2004 : PDGF-BB stimulated tyrosine phosphorylation of Jak-2 and STAT-3 in a time dependent manner in VSMCs ... In addition, AG490 and Jak-2KEpRK5, a selective pharmacological inhibitor and a dominant negative mutant, respectively, of Jak-2, attenuated PDGF-BB induced STAT-3 tyrosine phosphorylation and its DNA binding and reporter gene activities ... PDGF-BB induced the expression of cPLA(2) in a Jak-2/STAT-3 dependent manner, and pharmacological inhibitors of cPLA(2) prevented PDGFBB induced VSMC motility
Wu et al., Pharmacol Res 2009 (MAP Kinase Signaling System) : FBS- and PDGF-BB stimulated intracellular Ras, MEK1/2, ERK1/2, proliferative cell nuclear antigen ( PCNA ), and Akt activations were significantly inhibited by lercanidipine ; however, lercanidipine did not affect FBS- and PDGF-BB induced STAT3 phosphorylation
Lennartsson et al., J Biol Chem 2013 (Cell Transformation, Neoplastic...) : In cells in which Fer was down-regulated using siRNA, PDGF-BB was unable to induce phosphorylation of STAT3 , whereas phosphorylations of STAT5, ERK1/2, and Akt were unaffected ... PDGF-BB induced activation of STAT3 occurred also in cells expressing kinase-dead Fer, suggesting a kinase independent adaptor role of Fer ... Our data suggest a critical role of Fer in PDGF-BB induced STAT3 activation and cell transformation
Garcia et al., Cell Growth Differ 1997 (Breast Neoplasms...) : In addition, Stat3 activation is induced by another nonreceptor tyrosine kinase, v-Fps ; by polyoma virus middle T antigen, which activates Src family kinases ; and by v-Sis , which acts as a ligand for the platelet derived growth factor receptor