Gene interactions and pathways from curated databases and text-mining

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AKT2 — IKBKG

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Romashkova et al., Nature 1999 : We show that, upon PDGF stimulation, Akt transiently associates in vivo with IKK and induces IKK activation
Madrid et al., Mol Cell Biol 2000 : Inhibition of IkappaB kinase (IKK), using an IKKbeta dominant negative protein, demonstrated that activated Akt requires IKK to efficiently stimulate the transactivation domain of the p65 subunit of NF-kappaB
Pianetti et al., Oncogene 2001 (Breast Neoplasms...) : Inhibition of Akt did not affect IKK activity
Shao et al., Cancer Res 2001 (Ovarian Neoplasms) : Thus, our results suggest that inhibition of IKK activity and IkappaB degradation is the predominant mechanism for E1A mediated inhibition of radiation induced NF-kappaB activity and that radiation induced Akt activation can not be inhibited by E1A and is likely independent of radiation induced NF-kappaB activity
Chen et al., J Biol Chem 2002 : Furthermore, a dominant negative mutant of Akt abolishes IKKbeta inhibition by CaMKKc and ionomycin, suggesting that Akt acts as a mediator of CaMKK signaling to inhibit IL-1beta induced IKK activity at an upstream target site
Inoue et al., Br J Pharmacol 2005 (Osteosarcoma) : The drug also partially inhibited the activity of IKK , but almost fully inhibited the phosphorylation of Akt and the production of PtdIns ( 3,4,5 ) P ( 3 )
Ouyang et al., Carcinogenesis 2006 (Skin Neoplasms) : Furthermore, inhibition of PI-3K/Akt by overexpression of Deltap85 or DN-Akt blocked arsenite induced IKK phosphorylation, IkappaBalpha degradation and cyclin D1 expression, indicating that IKK/NFkappaB is the downstream transducer of arsenite triggered PI-3K/Akt cascade
Takada et al., J Immunol 2006 : AKBA also did not directly modulate IKK activity but suppressed the activation of IKK through inhibition of Akt
Tong et al., Respir Res 2006 : In addition, HIMF strongly induced Akt phosphorylation, and suppression of Akt activation by specific inhibitors and dominant negative mutants for PI-3K, and IKK or IkappaBalpha blocked HIMF induced NF-kappaB activation and attenuated HIMF induced VEGF production
Noman et al., Innate Immun 2009 : Thalidomide prevented the activation of nuclear factor (NF)-KB by down regulating phosphorylation of inhibitory KB factor ( IKB ), and IKB kinase (IKK)-alpha and IKK-beta Moreover, thalidomide inhibited LPS induced phosphorylation of AKT , p38 and stress activated protein kinase ( SAPK ) /JNK
Ottonello et al., Br J Pharmacol 2009 : The activity of oxaprozin was related to inhibition of Akt activation that, in turn, prevented p38 MAPK, IKK and NF-kappaB activation
Reddy et al., J Cell Physiol 2011 (Hyperplasia) : In addition to inducing its own expression via phosphatidylinositol 3-kinase/Akt dependent IKK/NF-?B activation, IL-18 stimulated glycogen synthase kinase 3ß phosphorylation and degradation, ß-catenin nuclear translocation and stabilization, T-cell factor-lymphoid enhancer binding factor ( TCF-LEF ) activation, and WISP1 induction
Yang et al., Carcinogenesis 2012 (Ovarian Neoplasms) : In addition, the tectorigenin-paclitaxel combination inhibited the phosphorylation of I?B and IKK and the activation of Akt in paclitaxel-resistant cancer cells
Äijö et al., Bioinformatics 2013 (Carcinoma, Hepatocellular...) : Our analysis of the hepatocellular liver carcinoma data predict a regulatory connection where AKT activity is dependent on IKK in TGFa stimulated cells, which is supported by the original data but not included in the original model