Gene interactions and pathways from curated databases and text-mining

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AKT2 — GRAP2

Text-mined interactions from Literome

Bayle et al., J Biol Chem 2004 : SOCS6 reduced SCF induced activation of ERK1/2 and p38 but not activation of AKT or STATs in Ba/F3, murine embryonic fibroblast (MEF), or COS-7 cells
Shlapatska et al., Exp Oncol 2004 (Burkitt Lymphoma...) : The effect of DOX in drug-resistant cell line DG75 convoyed by dephosphorylation of JNK1/2, p38 MAPK and activation of Akt
Kobayashi et al., Exp Dermatol 2005 : We show ( i ) UV induced up-regulation of TNF-alpha mRNA and protein expression in keratinocytes ; ( ii ) cells treated with KTI before UV irradiation showed a significantly lower accumulation of TNF-alpha protein in a dose dependent manner and a reduced UV-induced up-regulation of TNF-alpha mRNA expression ; ( iii ) KTI inhibited the induction of TNF-alpha target molecules interleukin-1beta (IL-1beta) and IL-6 proteins ; ( iv ) UV irradiation transiently activated c-Jun N-terminal kinase (JNK) and Akt signaling but only weakly activated extracellular signal regulated kinase ( ERK ) and p38 ; ( v ) KTI specifically inhibited UV-induced activation of ERK, JNK, and p38 , but not Akt ; ( vi ) treatment of cells with SP600125, a pharmacological inhibitor of JNK, predominantly suppressed UV-induced up-regulation of TNF-alpha expression ; and ( vii ) KTI did not enhance suppression of UV-induced JNK phosphorylation by SP600125
Sunters et al., Cancer Res 2006 (Breast Neoplasms) : To further investigate its mechanism of action, we treated MCF-7 cells with paclitaxel and showed a dose dependent increase in nuclear localization of FOXO3a, which coincided with decreased Akt signaling but increased c-Jun NH2-terminal kinase 1/2 (JNK1/2), p38 , and extracellular signal regulated kinase 1/2 ( ERK1/2 ) activity
Shacka et al., Cell Death Differ 2006 : Selective inhibition of mixed lineage kinase (MLK), p38 or JNK does not attenuate the decrease in Akt phosphorylation showing that inactivation of the Akt pathway occurs independently of the MLK/MAPK pathway
Zhang et al., Am J Physiol Cell Physiol 2006 : Pertussis toxin ( PTX ) blocks LPA induced activation of p38 and ERK but only slightly inhibits LPA induced activation of Akt
Hu et al., J Biol Chem 2006 (MAP Kinase Signaling System) : MAPKAPK-2, Akt2 , and ezrin phosphorylation were all attenuated by p38 MAPK inhibition but were unaffected by dominant negative ezrin expression
Park et al., Cancer Res 2006 (Glioblastoma...) : In addition, inhibitors of epidermal growth factor receptor ( EGFR ; AG490 and AG1478 ), Src ( PP2 ), and p38 ( SB203580 ), EGFR neutralizing antibody, and transfection of DN-Src and DN-p38 significantly blocked IR-induced Akt phosphorylation and MMP-2 secretion
Charalambous et al., Carcinogenesis 2007 (Neoplasms) : This is accompanied by down-regulation of Akt and activation of caspase-3 and p38 mitogen activated protein kinase ( MAPK )
Diehl et al., J Surg Res 2007 (Breast Neoplasms...) : We show that EGF works as a survival signal in the absence of p38MAPK mediated activation of AKT
Mao et al., Biochem Pharmacol 2008 : Similar to SFLLRN, the TFRRR-peptide caused phosphorylation of Akt and Erk in a P2Y ( 12 ) receptor dependent manner, and p-38 MAP kinase activation in a P2Y ( 12 ) -independent manner
Lin et al., Rheumatol Int 2008 (Chondrosarcoma...) : Using chondrosarcoma cells stimulated with IL-1beta, the effects of GLN on the mRNA and protein levels of MMP-3, the activation of JNK, ERK, p38 , NF-kappaB, and AP-1, the nuclear translocation of NF-kappaB/Rel family members, and PI3-kinase/Akt activation were studied
Ruhland et al., Exp Parasitol 2009 : Interestingly, activation of PI3K/Akt signaling had differential effects on ERK and p38 activation
Kulasekaran et al., Am J Respir Cell Mol Biol 2009 (Idiopathic Pulmonary Fibrosis) : ET-1 induced activation of PI3K/AKT is dependent on p38 mitogen activated protein kinase ( MAPK ), but not extracellular signal regulated kinase ( ERK ) 1/2, JNK, or transforming growth factor (TGF)-beta1
Fu et al., J Vet Med Sci 2009 (Inflammation) : Vaspin did not inhibit the TNF-alpha ( 20 min ) activation of JNK, p38 and NF-kappaB, but only slightly inhibited Akt
He et al., Sichuan Da Xue Xue Bao Yi Xue Ban 2010 : Compared with the nomoxia control, hypoxia enhanced the proliferation of MRC-5 and the expressions of pro-collal, p-p38 and p-AKT ( P < 0.05 ). Curcumin inhibited the hypoxia induced proliferation of MRC and the expression of pro-collal and p-p38 ( P < 0.05 ), but not the expression of p-AKT ( P > 0.05 )
Perdiguero et al., J Cell Biol 2011 (Inflammation) : In the absence of MKP-1, p38 induced AKT activity anticipated the acquisition of the antiinflammatory gene program and final cytokine silencing in macrophages, resulting in impaired tissue healing
Dai et al., J Biol Chem 2012 (Carcinoma, Hepatocellular...) : Both p38 MAPK promoted glucose regulated protein 78 (GRP78) expression and sustained high basal activation of PI3K/Akt and MEK/ERK are involved in the cytoprotective function of p190Met ( NC )
Hirabara et al., J Nutr Biochem 2013 : This effect was associated with increased insulin stimulated p38 MAP kinase phosphorylation and lower n-6/n-3 fatty acid ratio, but not with activation of proteins from insulin signaling ( IR, IRS-1 and Akt )
Jayakumar et al., J Nutr Biochem 2013 : Furthermore, a PI3-kinase inhibitor ( LY294002 ) and a p38 MAPK inhibitor ( SB203580 ) both significantly diminished PKC activation and p38 MAPK and Akt phosphorylation ; in contrast, a PKC inhibitor ( RO318220 ) did not diminish p38 MAPK or Akt phosphorylation stimulated by collagen
Shiragami et al., Int J Oncol 2013 (Colonic Neoplasms) : Cerulenin treatment was associated with reduced levels of phosphorylated Akt , activation of p38 and induced caspase-3 cleavage and finally caused apoptosis
Berra et al., J Biol Chem 1998 : Consistent with this, expression of active mutants of PI 3-kinase and Akt inhibits p38 activation and apoptosis