Gene interactions and pathways from curated databases and text-mining

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RAC1 — STAT3

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Turkson et al., Mol Cell Biol 1999 (Cell Transformation, Neoplastic...) : Expression of Ras or Rac1 dominant negative protein blocks Stat3 mediated gene regulation induced by Src in a manner consistent with dependence on p38 and c-Jun N-terminal kinase (JNK)
Schuringa et al., Biochem J 2000 (Carcinoma, Hepatocellular...) : Interleukin-6 induced STAT3 transactivation and Ser727 phosphorylation involves Vav, Rac-1 and the kinase SEK-1/MKK-4 as signal transduction components
Simon et al., Science 2000 : Dominant negative Rac1 inhibited STAT3 activation by growth factors, whereas activated Rac1 stimulated STAT3 phosphorylation on both tyrosine and serine residues
Faruqi et al., Proc Natl Acad Sci U S A 2001 : Rac1 mediates STAT3 activation by autocrine IL-6 ... The activity of Rac1 leads to STAT3 translocation to the nucleus coincident with STAT3 dependent gene expression ... Our studies indicate that Rac1 induces STAT3 activation through an indirect mechanism that involves the autocrine production and action of IL-6, a known mediator of STAT3 response ... Rac V12 expression results in the induction of the IL-6 and IL-6 receptor genes and neutralizing antibodies directed against the IL-6 receptor block Rac1 induced STAT3 activation ... Furthermore, inhibition of the nuclear factor-kappaB activation or disruption of IL-6 mediated signaling through the expression of IkappaBalpha S32AS36A and suppressor of cytokine signaling 3, respectively, blocks Rac1 induced STAT3 activation
Pelletier et al., Mol Cell Biol 2003 : We further show that GPCR agonists stimulate tyrosine phosphorylation of STAT1 and STAT3 proteins in a Rac dependent manner
Mamidipudi et al., Mol Cell Biol 2004 (Neoplasms) : We also show that Stat3 is required for Rac1 induction of Myc
Park et al., J Immunol 2004 : Rac1 contributes to maximal activation of STAT1 and STAT3 in IFN-gamma stimulated rat astrocytes
Debidda et al., J Biol Chem 2005 (Inflammation) : We also found that although active RhoA, Rac1 , and Cdc42 could all mediate Ser-727 and Tyr-705 phosphorylation and nuclear translocation of STAT3 , the Rho GTPases were able to induce STAT3 activation independently of the interleukin-6 autocrine pathway, and active RhoA, Rac1, or Cdc42 could not form a stable complex with STAT3 as previously suggested, indicating an unappreciated mechanism of STAT3 activation by the Rho GTPases
Yang et al., Arterioscler Thromb Vasc Biol 2005 (Myocardial Reperfusion Injury) : In cultured human umbilical vein endothelial ( HUVE ) cells, activation of Stat3alpha after hypoxia-reoxygenation ( H-R ) was dependent on the small GTPase Rac1
Tsai et al., Circulation 2008 (Atrial Fibrillation...) : In atrial myocytes, activation of STAT3 by Rac1 was mediated by direct association of Rac1 with STAT3 ; however, in atrial fibroblasts, it was mediated by an indirect paracrine effect
Simeone-Penney et al., Am J Physiol Lung Cell Mol Physiol 2008 : Additionally, PDGF induced activation of STAT3 required the small GTP binding protein Rac1 , and Rac1 was also required for PDGF induced HASMC proliferation
Tsai et al., Heart Rhythm 2008 (Atrial Fibrillation) : Membrane translocation of small GTPase Rac1 and activation of STAT1 and STAT3 in pacing induced sustained atrial fibrillation
Arulanandam et al., Exp Cell Res 2010 : Knockdown of gp130, the common subunit of this family reduced Stat3 activity, indicating that these cytokines may be responsible for the Stat3 activation by Rac ( V12 )
Teng et al., J Cell Sci 2009 : Through rescue experiments, we demonstrate that Stat3 can regulate the activation of Rac1 to mediate persistent directional migration and that this function is not dependent on Stat3 transcriptional activity ... We find that Stat3 binds to betaPIX, a Rac1 activator, and that this interaction could represent a mechanism by which cytoplasmic Stat3 regulates Rac1 activity to modulate the organization of actin cytoskeleton and directional migration
Banerjee et al., Cancer Res 2010 : STAT3 was regulated in NF1-deficient cells of murine and human origin in a TORC1- and Rac1 dependent manner
Ock et al., Cancer prevention research (Philadelphia, Pa.) 2011 (Colitis...) : Supported with the facts that Rac1 binds and activates STAT3 , which are significantly upregulated in inflammatory bowel disease ( IBD ) as well as CAC, but 8-hydroxydeoxyguanosine ( 8-oxo-7,8-dihydrodeoxyguanosine or 8-OHdG ) paradoxically can block Rac1 activation and subsequent NADPH oxidase ( NOX ) inactivation in various inflammation models, we hypothesized that attenuated Rac1-STAT3 and COX-NF-?B pathway by exogenous 8-OHdG administration may ameliorate inflammatory signaling in dextran sodium sulfate (DSS) induced colitis and can prevent CAC
Mattagajasingh et al., Biochim Biophys Acta 2012 : Activation of Stat3 in endothelial cells following hypoxia-reoxygenation is mediated by Rac1 and protein Kinase C