◀ Back to AKT1

AKT1 — CRK

Pathways - manually collected, often from reviews:

• WikiPathways Insulin Signaling: GSK3B/AKT2/AKT1/SGK3/SGK1/GSK3A/PDPK1/SGK2 → STXBP2/CYTH3/KIF5B/EHD2/ARF6/RAB4A/CAP1/STXBP1/CRK/STXBP4/TBC1D4/SH2B2/EHD1/ARHGAP33/STX4/SNAP25/RHOQ/SNAP23/CBLB/STXBP3/CBL/FLOT2/CBLC/MYO1C/RHOJ/SORBS1/ARF1/RAPGEF1/VAMP2/FLOT1/KIF3A (activation)
  

Text-mined interactions from Literome

Nelson et al., J Biol Chem 2001 : These data indicate that suppression of Akt and MAPK in the presence of activated p38 results in cell death and a possible mechanism for the enhanced apoptosis produced by the combination of CI-1033 and gemcitabine in MDA-MB-453 cells
Akagi et al., Mol Cell Biol 2002 : The v-Crk induced activation of AKT was greatly enhanced by the overexpression of H-Ras or its guanine nucleotide exchange factor mSOS, which binds to the v-Crk SH3 domain, whereas a dominant negative mutant of H-Ras almost completely suppressed this activation
Kaplan-Albuquerque et al., J Biol Chem 2003 (MAP Kinase Signaling System) : Expression of myr-Akt selectively inhibited AVP induced activation of c-Jun N-terminal kinase and p38 mitogen activated protein kinases, which we have shown are critical for induction of these genes
Wu et al., Am J Physiol Lung Cell Mol Physiol 2005 : Inhibition of p38 , Src, and EGFR kinases with pharmacological inhibitors markedly reduces Akt phosphorylation induced by Zn2+
Naïmi et al., Endocrinology 2007 (MAP Kinase Signaling System) : In contrast, Foxo1-ADA increases p38 activity, and p38 is required for effects of Foxo1 on PKB , at least in part
Diehl et al., J Surg Res 2007 (Breast Neoplasms...) : We found that, in the absence of EGF, p38MAPK activated AKT is necessary for HER-2 overexpressing cells to survive and to form colonies in soft agar
Gills et al., J Biol Chem 2007 : Although PIAs rapidly activated p38 with similar time and dose dependence as Akt inhibition, p38 activation and Akt inhibition were independent events induced by PIAs
Bouchard et al., Apoptosis 2008 : We report that : ( 1 ) Anoikis causes a down-activation of Fak, Src, Akt-1 and Erk1/2, a loss of Fak-Src association, and a sustained/enhanced activation of p38beta , which is required as apoptosis/anoikis driver ; ( 2 ) PI3-K/Akt-1 up-regulates the expression of Bcl-X ( L ) and Mcl-1, down-regulates Bax and Bak, drives Bad phosphorylation ( both serine112/136 residues ) and antagonizes p38beta activation ; ( 3 ) MEK/Erk up-regulates Bcl-2, drives Bad phosphorylation ( serine112 residue ), but does not antagonize p38bactivation ; ( 4 ) PI3-K/Akt-1 is required for survival, whereas MEK/Erk is not ; ( 5 ) Src acts as a cornerstone in the engagement of both pathways by beta1 integrins/Fak, and is crucial for survival ; and ( 6 ) beta1 integrins/Fak and/or Src regulate Bcl-2 homologs as both PI3-K/Atk-1 and MEK/Erk combined ... Hence, beta1 integrin/Fak/Src signaling translates into integrated mediating functions of p38beta activation and regulation of Bcl-2 homologs by PI3-K/Akt-1 and MEK/Erk, consequently determining their requirement ( or not ) for survival
Kim et al., Oncogene 2009 : Akt2, but not Akt1 , is required for cell survival by inhibiting activation of JNK and p38 after UV irradiation
Kozono et al., Biochem Biophys Res Commun 2010 : CP55940 ( CB1/CB2 agonist ) induced phosphorylation of the extracellular regulated kinases (ERK) 1/2, p38 mitogen activated protein kinase ( p38MAPK ), and Akt in HGFs. Wound closure by CP55940 in an in-vitro scratch assay was significantly suppressed by inhibitors of MAP kinase kinase ( MEK ), p38MAPK , and phosphoinositol 3-kinase (PI3-K)
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 )
Samoylenko et al., Carcinogenesis 2012 (Adenocarcinoma...) : Thereby, Ruk ( l ) /CIN85 led to a more rapid and prolonged epidermal growth factor dependent activation of Src, Akt and ERK1/2 and treatment with the Src inhibitor PP2 and the PI3K inhibitor LY294002 abolished the Ruk ( l ) /CIN85 dependent changes in cell motility
Li et al., Retrovirology 2013 : Activation of Erk/Akt suppresses p38 due to CCR5 binding, and allows cell survival