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RHOA — SMN1
Text-mined interactions from Literome
Morishita et al., J Neurochem 2007
:
Transfection of active forms of RhoA and its effector, mDia, strongly enhanced
SMA promoter activity, and a dominant negative form of
RhoA inhibited endothelin stimulated promoter activity but not TGF-beta stimulated activity
Mondin et al., Biochem Pharmacol 2007
:
Pharmacological inhibition of
RhoA activity
reduced expression of both SMA and calponin, whereas overexpression of a dominant negative form of Rac1 increased
SMA expression
Grabski et al., Arterioscler Thromb Vasc Biol 2009
(Carotid Artery Injuries) :
S1P stimulated
SMA expression
requires S1P2R dependent activation of
RhoA and mobilization of calcium from intracellular stores ... We further conclude that transcriptional regulation of
SMA by S1P in vitro
requires S1P2R dependent activation of
RhoA and mobilization of calcium from intracellular calcium stores
Fintha et al., Am J Pathol 2013
(Diabetic Nephropathies...) :
When co-expressed, it inhibited the stimulatory
effects of MRTF-A, MRTF-B or the constitutive active forms of
RhoA , Rac1, or Cdc42 on the
SMA promoter