Gene interactions and pathways from curated databases and text-mining

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RHOA — SLC22A3

Text-mined interactions from Literome

Bhowmick et al., Mol Biol Cell 2001 : In contrast, we show that TGF-beta rapidly activates RhoA in epithelial cells, and that blocking RhoA or its downstream target p160(ROCK), by the expression of dominant negative mutants, inhibited TGF-beta mediated EMT
Tavares et al., Dev Dyn 2006 : We explore here whether RhoA mediates this EMT
Patel et al., Am J Nephrol 2006 : Inhibition of EMT in HK2 cells with these statins resulted in a reduction of RhoA and Rac1 activation in both the cytoplasmic and membrane bound forms, in preservation of the expression of the epithelial cell markers E-cadherin and cytokeratin-19, and in a decrease in Fn-EDA expression, a marker for the myofibroblast phenotype
Townsend et al., J Biol Chem 2008 : Decreasing RhoA activity using dominant negative RhoA or small interfering RNA in ventricular endocardial cells also increases EMT, whereas overexpression of constitutively active RhoA in AVC endothelial cells blocks EMT ... These data demonstrate a functional role for Par6/Smurf1/RhoA in regulating EMT in endocardial cells
Tang et al., Hepatology 2010 (Carcinoma, Hepatocellular...) : Conclusion : EIF5A2 plays an important role in HCC invasion and metastasis by inducing EMT , as well as stimulating cytoskeleton rearrangement through activation of RhoA and Rac1
Sánchez et al., Cell Signal 2012 : TGFßR3 dependent endocardial EMT stimulated by either TGFß2 or BMP-2 requires activation of the Par6/Smurf1/RhoA 1pathway where Activin Receptor Like Kinase ( ALK5 ) signals Par6 to act downstream of TGFß to recruit Smurf1 to target RhoA for degradation to regulate apical-basal polarity and tight junction dissolution