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HSPG2 — PRKAR2B

Text-mined interactions from Literome

Alava et al., Biochem J 1992 : These results suggest that PKA mediated phosphorylation of PLC may regulate TCR/CD3 induced InsPL hydrolysis
Orihuela et al., J Endocrinol 2006 (MAP Kinase Signaling System) : Inhibition of adenylyl cyclase by i.b. injection of SQ 22536 blocked the increase of IP3 levels induced by E ( 2 ), while inhibition of PLC by ET-18-OCH ( 3 ) had no effect on E ( 2 ) -induced PKA activity ... Thus, activation of PLC-IP3 by E ( 2 ) requires previous stimulation of cAMP-PKA
Lee et al., Glia 2006 : The H2S induced calcium elevation is partly attenuated by H-89, a selective cAMP dependent protein kinase (PKA) inhibitor , but not by U73122, a phospholipase C (PLC) inhibitor, and chelerythrine, a selective protein kinase C ( PKC ) inhibitor, suggesting the involvement of cAMP/PKA, but not PLC/PKC/phosphoinositol-3,4,5-inositol ( IP3 ) pathway
Li et al., Clinical calcium 2006 (Osteochondrodysplasias) : Signaling transduction through the PTH/PTHrP receptor has two possible pathways : the activation of adenylate cyclase and subsequent protein kinase A (PKA) , and the activation of phospholipase C (PLC)
Moniri et al., Neurosci Lett 2006 : Results for cis-PAB suggest H1/PLC/IP/DAG/PKC signaling activates PKA , downstream of cAMP formation, indicating apparent direct activation of PKA by PKC
Tawfeek et al., Endocrinology 2008 : In the current study, we explored the role of PTH/PTHrP receptor phosphorylation and PKA in PTH activation of PLC
Chu et al., Chin J Physiol 2009 (Heart Diseases) : Moreover, immunoprecipitation assay revealed that treatment with IGF-II could enhance the interaction of IGF2R with Galphai and Galphaq but reduce its binding with Galphas, resulting in the reduction of phospho-PKA and the activation of PLC-beta
Kennedy et al., Biochim Biophys Acta 1995 : Regulation of phospholipases C (PLC) and arachidonic acid ( AA ) release by cAMP dependent protein kinase (PKA) was investigated in MDCK-D1 cells ... The results strongly suggest a role for PKA in the regulation of PLC activity and AA release in MDCK-D1 cells
Murphy et al., Biochem Biophys Res Commun 1994 : These results imply that H-ras functions, in this system, to decrease levels of cAMP, thus negating the regulatory effect of PKA on PLC
Yu et al., J Biol Chem 1996 : The fenoldopam induced increase in PLC-gamma and activity was mediated by protein kinase A (PKA) since it was blocked by the PKA antagonist Rp-8-CTP-adenosine cyclic 3 ' : 5'-monophosphorothioate ( Rp-8-CTP-cAMP-S ) and mimicked by direct stimulation of adenylyl cyclase with forskolin or by a PKA agonist, Sp-cAMP-S ... We suggest that the D1A mediated stimulation of PLC occurs as a result of PKA activation ... PKA then stimulates PLC-gamma in cytosol and membrane via activation of PKC
Ding et al., Cell Signal 1997 : Furthermore, elevation of cAMP may inhibit IP3 production and [ Ca2+ ] i mobilization through mechanisms involving PKA dependent phosphorylation of PLC , G-proteins, IP3 receptor and/or IP3 metabolizing enzymes