Gene interactions and pathways from curated databases and text-mining

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AKT2 — 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 ... 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