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PRKAR1A — RHOA
Text-mined interactions from Literome
Thibault et al., J Leukoc Biol 2002
:
The activator of
protein kinase A (PKA) , Sp-cAMP
inhibited fMLP induced PLD activation and translocation of Arf and
RhoA to membranes
Leemhuis et al., J Pharmacol Exp Ther 2002
:
Activated
protein kinase A (PKA) inhibits
RhoA and induces extensions
Qiao et al., Am J Physiol Lung Cell Mol Physiol 2003
:
PKA inhibits
RhoA activation : a protection mechanism against endothelial barrier dysfunction ... In conclusion, the results provide evidence that
PKA inhibited
RhoA activation in endothelial cells, supporting a signaling mechanism of protection against vascular endothelial barrier dysfunction
Jang et al., Exp Mol Med 2004
:
These results suggest that both PLD1 and RhoA are phosphorylated by
PKA and the interaction between PLD1 and
RhoA is
inhibited by the phosphorylation of RhoA rather than by the phosphorylation of PLD1
Zhang et al., Am J Physiol Gastrointest Liver Physiol 2005
(Hypertension, Portal) :
Acute inhibition of
PKA had no effect on
RhoA mRNA expression
Chen et al., Experimental biology and medicine (Maywood, N.J.) 2005
(Prostatic Neoplasms) :
Results of this experiment indicated that
cAMP/PKA inhibited
RhoA activation, and serine188 phosphorylation on RhoA was necessary for PKA to exert its inhibitory effect on RhoA activation
Park et al., Dev Biol 2006
:
As a negative component of PCP signaling,
PKA inhibits not only the activation of
RhoA and JNK but also the Dsh-Daam1-RhoA complex formation which is essential for the regulation of RhoA activity
Wang et al., Oncol Rep 2006
:
AKAPs competing peptide HT31 disrupts the inhibitory
effect of
PKA on
RhoA activity ... The results showed that HT31 not only blocked the
PKA induced phosphorylation of
RhoA but also prevented the PKA induced inhibition on RhoA activation
Cardone et al., PloS one 2008
(Cell Transformation, Viral) :
Further, using pharmacological agents and transient transfections with dominant interfering, constitutively active, phosphorylation negative mutants and siRNA strategy to modify specific upstream signal transduction components that link HPV16 E7 oncogenic signals to up-regulation of the NHE1, we demonstrate that the stimulation of NHE1 activity is driven by an early rise in cellular cAMP resulting in the down-stream inhibition of p38 MAPK via the
PKA dependent phosphorylation of the small G-protein,
RhoA , and its subsequent inhibition
Li et al., Mol Med Report 2011
(Adenocarcinoma...) :
Results from laboratories, including ours, have demonstrated that
PKA inhibits the activity and function of
RhoA
O'Connor et al., Am J Physiol Cell Physiol 2012
:
Finally, we find that the regulation of Rac1 and
RhoA in response to LPA is differentially
regulated by phosphodiesterases,
PKA , and phosphatidylinositol 3-kinase, thus supporting their spatially distinct compartmentalization
Jones et al., Cell Signal 2012
:
Consistent with these observations, cAMP elevation triggered the
PKA dependent phosphorylation of
RhoA on serine 188, and a non-phosphorylatable Ser188Ala RhoA mutant functioned as a dominant negative inhibitor of cAMP mediated neuroendocrine phenotype formation ... These results suggest that
PKA mediated inhibition of
RhoA via its phosphorylation on serine 188 and the subsequent inhibition of ROCK activity plays a key role in determining initial changes in cellular morphology during LNCaP cell differentiation to a neuroendocrine phenotype
Oishi et al., J Biol Chem 2012
:
Protein kinase A (PKA) inhibits
RhoA signaling and thereby induces a characteristic morphological change, cell rounding ... Here we show that phosphorylation of RhoGDIa but not RhoA plays an essential role in the
PKA induced inhibition of
RhoA signaling and in the morphological changes using cardiac fibroblasts
Jia et al., Endocrinology 2013
:
Inhibition of
PKA significantly
attenuated the effect of genistein on thrombin induced EC permeability, MLC phosphorylation, and
RhoA membrane translocation in ECs ... These findings demonstrated that genistein improves thrombin induced endothelial barrier dysfunction in ECs through
PKA mediated suppression of
RhoA signaling
Rajagopal et al., Am J Physiol Gastrointest Liver Physiol 2013
:
OA, but not a selective exchange protein activated by cAMP ( Epac ) ligand ( 8-pCPT-2'-O-Me-cAMP ), caused phosphorylation of
RhoA and the phosphorylation was
blocked by the
PKA inhibitor, myristoylated PKI, and by the expression of phosphorylation-deficient mutant RhoA ( S188A ) ... We conclude that activation of TGR5 causes relaxation of gastric smooth muscle and the relaxation is mediated through inhibition of RhoA/Rho kinase pathway via both cAMP/Epac dependent stimulation of Rap1 and
cAMP/PKA dependent phosphorylation of
RhoA at Ser ( 188 )