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AKT3 — BAD
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
BAD
→
AKT3
(decreases, AKT3 Activity, BAD Activity)
Laine et al., J Biol Chem 2002*
Evidence: Modified assertion
-
KEGG Apoptosis:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG VEGF signaling pathway:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Neurotrophin signaling pathway:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Insulin signaling pathway:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Toxoplasmosis:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Tuberculosis:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Hepatitis C:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Pathways in cancer:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Colorectal cancer:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, phosphorylation)
-
KEGG Pancreatic cancer:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Endometrial cancer:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Prostate cancer:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Melanoma:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Chronic myeloid leukemia:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Acute myeloid leukemia:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Non-small cell lung cancer:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG Non-small cell lung cancer:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
KEGG ErbB signaling pathway:
AKT1/AKT2/AKT3
→
BAD
(protein-protein, inhibition)
-
WikiPathways ErbB Signaling Pathway:
AKT3
→
BAD
(inhibition)
-
WikiPathways Focal Adhesion-PI3K-Akt-mTOR-signaling pathway:
AKT1/AKT3/AKT2
→
BAD
(inhibition)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
STRING interaction:
AKT3
—
BAD
(interaction, mapped from bind)
-
STRING interaction:
BAD
—
AKT3
(interaction, mapped from bind)
Text-mined interactions from Literome
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
Stronach et al., Neoplasia (New York, N.Y.) 2011
(Carcinoma...) :
Resensitization is associated with prevention of
AKT mediated
BAD phosphorylation