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SOAT1 — SRC

Text-mined interactions from Literome

Sachsenmaier et al., Oncogene 1999 : STAT activation by the PDGF receptor requires juxtamembrane phosphorylation sites but not Src tyrosine kinase activation ... Consistent with a role for Src in STAT activation, we found that a PDGF receptor juxtamembrane tyrosine residue required for Src activation is necessary and sufficient for activation of STATs 1 and 3
Hartley et al., J Biol Chem 2000 : Furthermore, we demonstrate that, similar to STAT activation by v-Src , the optimum induction of STAT dependent transcription by Tip requires Ras/Rac mediated signaling events
Iwamoto et al., Oncogene 2000 (Acute-Phase Reaction) : The JAK-inhibitor, JAB/SOCS-1 selectively inhibits cytokine induced, but not v-Src induced JAK-STAT activation ... In this report, we investigated the effect of ectopic expression of JAB on v-Src induced JAK-STAT activation
Senga et al., J Biol Chem 2001 (Leukemia, Myeloid) : Recently, it was proven that Ral regulates c-Src activity and subsequent phosphorylation of its substrate, STAT3
Simon et al., Am J Physiol Lung Cell Mol Physiol 2002 : Inhibition of the Src and JAK kinases blocked PDGF stimulated gene expression of the STAT target genes cyclin D1 and c-myc
Krejci et al., J Cell Sci 2008 : Moreover, addition of active STAT1 and STAT3 to the FGF signal, by means of cytokine treatment, SRC mediated STAT activation or expression of constitutively active STAT mutants does not sensitize RCS chondrocytes to FGF mediated growth arrest
Beyer et al., PLoS Comput Biol 2011 : For IL-2R signaling, we show that STAT activation is independent of both Src- and PI3-kinases, while ERK activation depends upon both kinases and additionally requires novel PKCs