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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