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GNA15 — STAT3

Text-mined interactions from Literome

Wu et al., Biochem Biophys Res Commun 2003 (MAP Kinase Signaling System) : Agonist induced STAT3 activity required coexpression of G alpha(16) and was resistant to PTX treatment
Lo et al., J Biol Chem 2003 : In the present study, we have delineated the mechanism by which Galpha16 stimulates STAT3 in human embryonic kidney 293 cells ... Galpha16QL induced STAT3 activation was enhanced by overexpression of extracellular signal regulated kinase 1 ( ERK1 ), but was inhibited by U0126, a Raf-1 inhibitor, and coexpression of the dominant negative mutants of Ras and Rac1 ... Inhibition of phospholipase Cbeta, protein kinase C, and calmodulin dependent kinase II by their respective inhibitors also suppressed Galpha16QL induced STAT3 activation ... The involvement of tyrosine kinases such as c-Src and Janus kinase 2 and 3 ( JAK2 and JAK3 ) in Galpha16QL induced activation of STAT3 was illustrated by the combined use of selective inhibitors and dominant negative mutants ... Collectively, these results highlight the important regulatory roles of the Ras/Raf/MEK/ERK and c-Src/JAK pathways on the stimulation of STAT3 by activated Galpha16 ... Demonstration of the involvement of different kinases in Galpha16QL induced STAT3 activation supports the involvement of multiple signaling pathways in the regulation of transcription by G proteins
Liu et al., J Biol Chem 2006 : In contrast to the Galpha16 mediated regulation of STAT3 in HEK 293 cells ( Lo, R. K., Cheung, H., and Wong, Y. H. ( 2003 ) J. Biol. Chem. 278, 52154-52165 ), the Galpha ( s ) -mediated responses, including STAT3-driven luciferase activation, were resistant to inhibition of phospholipase Cbeta
Yeung et al., Cell Signal 2009 : In the presence of p63RhoGEF, Galpha(16)QL induced STAT3 phosphorylation was significantly reduced and Galpha(16)QL mediated SRE transcriptional activation was attenuated