◀ Back to PRKAR1A

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 )