Gene interactions and pathways from curated databases and text-mining

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AKT1 — BAD

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Fang et al., Oncogene 1999 (MAP Kinase Signaling System) : It has been shown that phosphorylation of BAD at Ser-136 is mediated by the serine/threonine protein kinase Akt-1/PKB which is downstream of phosphatidylinositol 3-kinase (PI3K)
Hila et al., Glia 2001 (Polyradiculoneuropathy) : PI-3 kinase-Akt pathway activation by C5b-9 induced, within 15 min, a 6.34 +/- 1.2-fold increase in BAD phosphorylation at Ser 136, but not at Ser 112
Trencia et al., Mol Cell Biol 2003 (Glioma) : Serum activation of Akt as well as BAD phosphorylation by Akt showed no difference in 293 cells transfected with PED/PEA-15 and in untransfected cells ( which express no endogenous PED/PEA-15 )
Li et al., Oncogene 2003 (Melanoma) : On the other hand, overexpression of MelCAM activated endogenous AKT and inhibited proapoptotic protein BAD in melanoma cells, leading to increased survival under stress conditions
Neithardt et al., J Cell Physiol 2006 : Overexpression of dominant negative Akt attenuated agonist induced phosphorylation of BAD , but not that of ERK1/2 and CREB
Claerhout et al., J Invest Dermatol 2007 : These data indicate that AKT induced BAD phosphorylation and its subsequent cytoplasmic sequestration by 14-3-3zeta is a major mechanism responsible for the postponement of UVB induced apoptosis in human keratinocytes
Henley et al., Cancer Chemother Pharmacol 2007 (Breast Neoplasms) : PTX induced JNK activity or AKT mediated BAD phosphorylation was unaffected by cell cycle inhibitors
Lue et al., Oncogene 2007 (Breast Neoplasms...) : Akt activation by MIF led to phosphorylation of the proapoptotic proteins BAD and Foxo3a
Raufman et al., J Cell Physiol 2008 (Colonic Neoplasms) : DCT induced PI3K/Akt activation resulted in downstream phosphorylation of GSK-3 ( Ser ( 21/9 ) ) and BAD ( Ser ( 136 ) ), and nuclear translocation ( activation ) of NF-kappaB, thereby confirming that DCT induced activation of PI3K/Akt signaling regulates both proproliferative and prosurvival signals
Wehr et al., BMC biotechnology 2008 : We also measured the phosphorylation dependent Bad/14-3-3 interactions mediated by endogenous and transient Akt-1 activity
Stronach et al., Neoplasia (New York, N.Y.) 2011 (Carcinoma...) : Resensitization is associated with prevention of AKT mediated BAD phosphorylation