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AKT1 — GDF15
Text-mined interactions from Literome
Campbell et al., J Biol Chem 2001
(Breast Neoplasms) :
Moreover,
AKT overexpression
led to up-regulation of estrogen regulated pS2 gene, Bcl-2, and
macrophage inhibitory cytokine 1
Sawyer et al., Circulation 2002
:
NRG-1beta ( 10 ng/mL )
activated erbB2, Erk1/2, and
Akt in ARVMs and significantly reduced anthracycline induced disarray
Fukazawa et al., J Mol Cell Cardiol 2003
:
NRG-1beta treatment
induced rapid activation of
Akt/PKB that was inhibited by wortmannin, and adenoviral mediated overexpression of a dominant negative Akt prevented the protective effect of NRG-1beta ...
Akt activation by
NRG-1beta was prevented by the tyrphostin AG1478, which we show inhibits erbB4 activation by NRG-1beta ... In contrast, the erbB2-specific tyrphostin AG879 had no effect on
NRG-1beta activation of
Akt
Lemmens et al., Circulation 2004
:
In cultured rat cardiomyocytes,
NRG-1beta enhanced nitrite production and
resulted in phosphorylation of endothelial NO synthase and the serine/threonine kinase
Akt
Yamaguchi et al., J Biol Chem 2004
:
PI3K inhibition by LY294002 showed an increase in
NAG-1 protein and mRNA expression, and 1l-6-hydroxymethyl-chiro-inositol 2 ( R ) -2-O-methyl-3-O-octadecylcarbonate (
AKT inhibitor ) also
induced NAG-1 expression
Wollmann et al., Carcinogenesis 2005
(Breast Neoplasms) :
MIC-1 activates the survival kinase
AKT/PKB in neuronal cells ... In this study, we show that
AKT/PKB directly
regulates the expression of
MIC-1 in breast cancer cells ... In this study, we show that
AKT/PKB directly
regulates the expression of
MIC-1 in breast cancer cells ... Sequences within -88 to +30 of the MIC-1 promoter are required for the
AKT mediated induction of
MIC-1 ... Mutation of SP-1C but not SP-1B reduced the
AKT mediated
activation of
MIC-1
Ritch et al., Glia 2005
(Astrocytoma...) :
Moreover,
Nrg-1beta activates an inhibitor of apoptosis,
Akt , implying a possible role for this kinase in mediating Nrg-1beta effects in gliomas
Nakaoka et al., J Clin Invest 2007
(Cardiovascular Abnormalities...) :
NRG-1beta induced
activation of both ERK and
AKT in the hearts of control mice but not in those of DKO mice
Shim et al., Mol Cancer Ther 2008
(Prostatic Neoplasms) :
Pretreatment with p38 kinase inhibitor blocked the VES induced increase in NAG-1 protein and mRNA levels, whereas an inhibition of protein kinase C,
Akt , c-Jun NH ( 2 ) -terminal kinase, or MEK activity
had no effect on VES induced
NAG-1 levels
Wang et al., Medical & biological engineering & computing 2009
:
Western blot analysis confirmed that the expression of
phospho-Akt in the beating foci was increased in the
presence of
NRG-1
Guo et al., Biochem Cell Biol 2010
(Brain Ischemia) :
Our results showed that recombinant human NRG-1 ( 3.0 ng.kg-1 ) significantly increased the expression of p-Akt protein, Bcl-2 mRNA, and the level of p-Bad, respectively, whereas administration of LY294002, a specific inhibitor of PI3K, significantly decreased the expression of
p-Akt , p-Bad, and Bcl-2
induced by
NRG-1 after a 60 min ischemic insult, followed by 24 h of reperfusion
Si et al., PloS one 2011
(Carcinoma, Hepatocellular...) :
Overexpressed
GDF15 led to
Akt activation and the phosphorylation of Akt downstream targeted GSK-3ß and Raf
Jie et al., Mol Cell Biochem 2012
(Ion Channel Gating) :
Taken together, these findings suggest that
NRG-1 activates
PI3K/Akt signaling and inhibits mPTP opening, and downstream apoptotic events in cardiac myocytes subjected to oxidative stress
Choi et al., Protein & cell 2012
(MAP Kinase Signaling System) :
While over expression of the intact human HER3 transformed CHO cells with oncogenic properties such as AKT/ERK activation and increased proliferation and migration, CHO cells expressing the HER3-2-3 chimeric receptor showed significantly reduced HER3/HER2 dimerization and decreased phosphorylation of both
AKT and ERK1/2 in the
presence of
neuregulin-1 (NRG-1) ... In contrast, CHO cells expressing the HER3-2-2 chimeric receptor resulted in a total loss of downstream
AKT activation in
response to
NRG-1 , but maintained partial activation of ERK1/2