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AKT1 — HSPG2
Text-mined interactions from Literome
Hong et al., Biochem Biophys Res Commun 2001
:
In addition,
PLC-gamma1 activation was
independent of
Akt/protein kinase B ( Akt/PKB )
Tang et al., J Biol Chem 2002
(Astrocytoma...) :
The pathway linking PLC coupled receptors to PI 3-kinase was deduced to involve phosphoinositide hydrolysis and Ca2+ dependent ErbB3 transactivation but not protein kinase C on the basis of the following evidence : ( i ) inhibition of carbachol stimulated
PLC by pretreatment with the phorbol ester phorbol 12-myristate 13-acetate concomitantly
reduced PKB activity, whereas stimulation of other PLC coupled receptors also activated
PKB ; ( ii ) Ca2+ ionophores and thapsigargin stimulated PKB activity in a wortmannin-sensitive manner, whereas bis ( 2-aminophenoxy ) ethane-N, N,N ', N'-tetraacetic acid blocked carbachol stimulated PKB activity ; ( iii ) phorbol 12-myristate 13-acetate alone did not activate PKB, whereas a protein kinase C inhibitor did not prevent the activation of PKB by carbachol ; and ( iv ) carbachol stimulated ErbB3-tyrosine phosphorylation and association with p85, and both these and PKB activity were blocked by tyrphostin AG1478, an epidermal growth factor receptor-tyrosine kinase inhibitor
Hassan et al., Regul Pept 2004
(Prostatic Neoplasms) :
The effects of NT on
EGFR/ERK/Akt activation and DNA synthesis were
attenuated by
PLC-inhibitor ( U73122 ), PKC-inhibitors ( bisindolylmaleimide, staurosporine, rottlerin ), MEK inhibitor ( U0126 ) and PI3 kinase inhibitors ( wortmannin, LY 294002 )
Liu et al., Endothelium : journal of endothelial cell research 2006
:
Contrarily, suppression of
PC-PLC promoted the phosphorylation of
Akt
Preiss et al., Cardiovasc Res 2007
:
Inhibitors of
phospholipase C (PLC) or classical PKCs as well as PKC depletion following phorbol ester treatments,
blocked Akt phosphorylation in response to PLA-LDL
Reséndiz et al., Journal of thrombosis and haemostasis : JTH 2007
:
Phospholipase C (PLC) controls
Akt phosphorylation elicited by PARs
Irino et al., J Neurosci Res 2008
:
These results indicate that
Akt activation is
dependent on the PI3K pathway and a
PLC mediated increase in intracellular calcium and suggest that Akt activation is involved in ADP induced microglial chemotaxis
Nakayama et al., J Biol Chem 2009
(Helicobacter Infections...) :
Methyl-beta-cyclodextrin (MCD) and phosphatidylinositol-specific phospholipase C (
PI-PLC ), but not 5-nitro-2- ( 3-phenylpropylamino ) -benzoic acid ( NPPB ) and bafilomycin A1,
inhibited VacA induced phosphorylation of
Akt , indicating that it does not require VacA internalization and is independent of vacuolation
Berna et al., Cell Signal 2009
(Pancreatic Neoplasms) :
However, GI-hormones/neurotransmitters [CCK, bombesin, carbachol ] activating
phospholipase C (PLC) inhibited basal and growth-factor stimulated
Akt activation
Kawashita et al., J Neurochem 2009
(Disease Models, Animal...) :
Furthermore, it was demonstrated that intracellular extracellular signal regulated kinase, c-Jun N-terminal kinase, and
phospholipase C (PLC) , but not phosphoinositide 3-kinase, should contribute to the induction of MIP-1alpha in SD-Mg, and that PLC could independently
regulate the activation of both PKC and
Akt
Chung et al., Exp Mol Med 2012
:
A
phospholipase C (PLC) inhibitor
blocked the increases in intracellular Ca ( 2+ ) levels, AMPK dependent eNOS phosphorylation, and NO production, but not
Akt activation, in syringaresinol- treated endothelial cells
Cao et al., PLoS Biol 2013
(Angelman Syndrome) :
In Ube3A deficient mice, the BDNF induced recruitment of PSD-95, as well as PLC? and Grb2 associated binder 1 (Gab1) with TrkB receptors was attenuated, resulting in reduced activation of
PLC?-a-calcium/calmodulin dependent protein kinase II ( CaMKII ) and
PI3K-Akt , but leaving the extracellular signal regulated kinase ( Erk ) pathway intact