◀ Back to AHSA1

AHSA1 — PRKAR1B

Text-mined interactions from Literome

Zheng et al., J Biol Chem 2000 : In contrast, a specific peptide inhibitor of PKA, PKI ( 5 microm ), completely abolished the stimulatory effect of beta ( 2 ) -AR, suggesting that beta ( 2 ) -AR induced p38 MAPK activation is mediated via a PKA dependent mechanism, rather than by G ( i ) or Gbetagamma
Schulte et al., Exp Cell Res 2003 : p38 activation by NECA was instead independent of PI3K but required cAMP and PKA
Mao et al., Exp Cell Res 2004 : Whereas PKA from cells treated with forskolin activated stress kinase p38, PKA from cells treated with sorbitol did not activate p38 , although the enzyme is activated in both cases as analysed in vitro using a specific peptide target
Rey et al., Bone 2007 (MAP Kinase Signaling System) : Activation of p38 is cAMP-PKA dependent and mediates PTH induced stimulation of ALP which plays a critical role for the calcification of the bone matrix
Tang et al., Cell Signal 2008 : ERK ( 1/2 ) activation involves Gq/phospholipase C (PLC)/protein kinase C ( PKC ), Gs/adenylyl cyclase ( AC ) /cAMP/protein kinase A (PKA) and Gi cascades ; however, the Gq/PLC/PKC pathway, as well as PKA is not required for OX2R mediated p38 MAPK activation
Cardone et al., PloS one 2008 (Cell Transformation, Viral) : HPV16 E7-dependent transformation activates NHE1 through a PKA-RhoA induced inhibition of p38alpha
Lajevic et al., Immunology 2011 (Thymoma) : p38 MAPK activation involves the ßAR, Gs protein, AC, cAMP and PKA , as determined through the use of a ßAR antagonist, activators of AC and cAMP, and S49 clonal mutants deficient in Gs and PKA