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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