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RHOA — TGFB1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Zhang et al., Cell Tissue Res 2002
:
In addition,
TGF-beta1 increases
RhoA activation and enhances actin condensation in HBMEC ...
TGF-beta1 increases E. coli K1 invasion in PI3K dominant negative HBMEC, but not in
RhoA dominant negative HBMEC, indicating that TGF-beta1 mediated increase in E. coli K1 invasion is RhoA dependent, but not PI3K dependent
Bartolomé et al., Mol Biol Cell 2003
:
Although
TGF-beta1 rapidly
activated the small GTPase
RhoA and the p38 mitogen activated protein kinase, enhanced adhesion did not require activation of both signaling molecules
Ito et al., Am J Pathol 2004
:
In the presence of HA,
TGF-beta1 mediated activation of
RhoA was also abrogated in a CD44 dependent manner
Imamichi et al., Biol Chem 2005
:
In addition to ERK and JNK, the monomeric GTPase
RhoA was
activated by
TGF beta1 and necessary for TGF beta induced migration
Han et al., J Clin Invest 2005
(Carcinoma in Situ...) :
However, Delta ( beta ) RII did not alter
TGF-beta1 mediated expression of
RhoA/Rac and MAPK, which contributed to increased metastasis
Lu et al., J Appl Physiol 2006
:
In this study, we hypothesized that
TGF-beta1 induced changes in endothelial monolayer permeability and in p38 and
RhoA activation are dependent on Smad2 signaling ... We assessed the role of Smad2 in p38 activation and the role of p38 in
RhoA activation by
TGF-beta1 ... Finally, inhibition of de novo protein expression blunted
TGF-beta1 induced
RhoA activation and endothelial barrier dysfunction
Kim et al., Blood 2006
:
TGF-beta1 activated
RhoA in the initial period, and thereafter inactivated them, suggesting that the inactivation of RhoA may be the cause of the reduced cell migration in response to TGF-beta1 at later times
Park et al., J Biol Chem 2006
:
TGFbeta(1) also
mediates a decrease in GTP bound
RhoA and a reciprocal increase in the expression of the RhoA GTPase activating protein, p190RhoGAP, whereas total RhoA is unchanged ... In contrast to atrial myocytes, in mink lung epithelial cells, in which TGFbeta signaling through activation of RhoA has been previously identified,
TGFbeta(1) stimulated an increase in GTP bound
RhoA in association with a reciprocal decrease in the expression of p190RhoGAP
Smith et al., J Periodontal Res 2006
(Gingivitis...) :
Our observations show that
TGF-beta1 activated the GTPase
RhoA , a key regulator of the actin cytoskeleton
Varon et al., Exp Cell Res 2006
:
Thus, Rac1 and
RhoA are
regulated by
TGFbeta1 in the process of endothelial tube formation in collagen I gels
Tumbarello et al., J Cell Physiol 2007
(Fibrosis...) :
In addition, Hic-5 siRNA treatment led to the suppression of
TGFbeta1 induction of
RhoA activation
Ganter et al., Circ Res 2008
(Pulmonary Edema...) :
The results of in vitro studies indicated that IL-1beta caused the activation of
transforming growth factor-beta via
RhoA/alphavbeta6 integrin
dependent mechanisms and the inhibition of the alphavbeta6 integrin and/or transforming growth factor-beta signaling completely blocked the IL-1beta mediated protein permeability across alveolar epithelial cell monolayers
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
Peng et al., American journal of physiology. Renal physiology 2008
:
TGFbeta1 induced
RhoA activation was prevented by disrupting caveolae with cholesterol depletion and rescued by cholesterol repletion ... Overexpression of nonphosphorylatable caveolin-1 Y14A prevented
TGFbeta1 induced
RhoA activation ...
TGFbeta1 also activated Src, and its inhibition
blocked RhoA activation ... Furthermore,
TGFbeta1 led to association of
RhoA and caveolin-1
Xing et al., Invest Ophthalmol Vis Sci 2009
:
TGFbeta1 also
activated RhoA and ROCK ( Y27632 ) inhibition reduced alpha-SMA expression
Hubchak et al., American journal of physiology. Renal physiology 2009
(Fibrosis) :
TGF-beta1 activated both
RhoA and Rac1 within 5 min of treatment, and this activation was dependent on the kinase activity of the type I TGF-beta receptor ... Thus, while both Rac1 and
RhoA are rapidly activated in
response to
TGF-beta1 in human mesangial cells, only Rac1 activation enhances events that contribute to mesangial cell collagen expression, through a positive feedback loop involving PI3K
Xing et al., Molecular vision 2009
:
The levels of pERK ( the extracellular signal regulated protein kinase ) and pSmad3 or the extent of the interaction between pSmad3 and CBP induced by TGFbeta1 were not affected by hypoxia whereas the activation of
RhoA induced by
TGFbeta1 was significantly reduced
Fernández-Calotti et al., J Biol Chem 2010
(Leukemia, Lymphocytic, Chronic, B-Cell...) :
TGF-beta1 acts through activation of ERK1/2 and the small GTPase
RhoA to promote plasma membrane trafficking of the hCNT3 protein
Lee et al., J Biol Chem 2010
:
Using small interfering RNAs, we found that NET1, the guanine nucleotide exchange factor of RhoA, is critical for
TGF-beta1 induced cytoskeletal reorganization, N-cadherin expression, and
RhoA activation