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CTGF — RHOA

Text-mined interactions from Literome

Iwanciw et al., Arterioscler Thromb Vasc Biol 2003 (Fibrosis) : Specific interference with RhoA signaling by Y27632 primarily reduced basal CTGF expression
Ott et al., J Biol Chem 2003 : Overexpression of constitutively active RhoA induced CTGF synthesis ... Interference with RhoA signaling by simvastatin, toxinB, C3 toxin, and Y27632 prevented up-regulation of CTGF
Chowdhury et al., Eur J Biochem 2004 (MAP Kinase Signaling System) : In particular, RhoA dependent regulation of the CTGF/CCN2 gene was concomitant to increased polymerization of actin microfilaments resulting in decreased G- to F-actin ratio and appeared to be achieved at the transcriptional level
Graness et al., Kidney Int 2006 : On the other hand, when the fibroblasts were cultured on a rigid matrix, that is collagen coated plates, strong focal complexes prevented the dynamic alterations, and RhoA mediated upregulation of CTGF expression was independent of Src-FAK signaling
Huang et al., Am J Physiol Lung Cell Mol Physiol 2006 : Modulation by bradykinin of angiotensin type 1 receptor evoked RhoA activation of connective tissue growth factor expression in human lung fibroblasts
Watts et al., Respir Res 2006 (Pulmonary Fibrosis) : We have previously shown that both CTGF overexpression and myofibroblast formation in IPF cell lines are dependent on RhoA signaling
Crean et al., FASEB J 2006 : CTGF also stimulated an increased association between Rho A and p27 ( Kip-1 )
Muehlich et al., Am J Physiol Cell Physiol 2007 : Overexpression of constitutively active RhoA or SRF significantly increased CTGF protein synthesis
Cicha et al., Atherosclerosis 2008 (Atherosclerosis) : Pharmacological inhibition of RhoA signaling prevents connective tissue growth factor induction in endothelial cells exposed to non-uniform shear stress ... In conclusion, non-uniform shear stress dependent CTGF expression requires active RhoA and can be prevented pharmacologically
Black et al., J Biol Chem 2008 : TGFbeta1 does not stimulate RhoA activation in gingival fibroblasts, and the overexpression of dominant negative RhoA does not reduce CCN2/CTGF expression in response to TGFbeta1
Samarin et al., J Biol Chem 2010 : Activation of RhoA-Rho kinase signaling by the microtubule disrupting drug combretastatin A4 also enhanced the DMOG induced CTGF expression, thus placing CTGF induction by hypoxia in a network of interacting signaling pathways
Iyer et al., Invest Ophthalmol Vis Sci 2012 : Expression of a constitutively active form of RhoA ( RhoAV14 ), activation of Rho GTPase by bacterial toxin, or inhibition of Rho kinase by Y-27632 in HTM cells led to significant but contrasting changes in CTGF protein levels that were detectable in cell lysates and cell culture medium