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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