◀ Back to AKT1
AKT1 — BAD
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
BAD
→
AKT1
(directlyDecreases, BAD Activity)
Giancotti et al., Science 1999
Evidence: FAK appears to play a major role in conveying survival signals from the ECM (50, 51). Because FAK binds PI 3-kinase, the protective effect against anoikis may be the result of PI 3-kinase-mediated activation of protein kinase B/Akt (52). Akt promotes survival, at least in part, by phosphorylating and thereby inactivating two proapoptotic proteins, Bad and caspase-9 (53) (Fig. 4). Inhibition of p53 prevents FAKdeficient cells from undergoing anoikis when deprived of growth factors, suggesting tha...
-
OpenBEL Selventa BEL large corpus:
BAD
→
AKT1
(increases, BAD Activity)
Evidence: In this paper, we present a comprehensive pathway map of EGFR signaling and other related pathways.
-
BioCarta il-2 receptor beta chain in t cell activation:
BAD
→
AKT (AKT1)
(apoptosis, activates)
-
BioCarta regulation of bad phosphorylation:
BAD/BCL-2 complex (BAD-BCL2)
→
AKT (AKT1)
(modification, collaborate)
-
BioCarta regulation of bad phosphorylation:
BAD/BCL-XL complex (BAD-BCL2L1)
→
AKT (AKT1)
(modification, collaborate)
-
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)
-
NCI Pathway Database ErbB1 downstream signaling:
BAD/BCL-XL complex (BAD-BCL2L1)
→
AKT1 (AKT1)
(modification, collaborate)
Romanelli et al., Mol Cell Biol 1999*, Jost et al., J Invest Dermatol 1999*, Romorini et al., Biochim Biophys Acta 2009*, Datta et al., Cell 1997*, Stoll et al., Oncogene 1998*
Evidence: assay
-
NCI Pathway Database Class I PI3K signaling events mediated by Akt:
BAD/BCL-XL complex (BAD-BCL2L1)
→
AKT1 (AKT1)
(modification, collaborate)
Datta et al., Cell 1997*, del Peso et al., Science 1997*
Evidence: mutant phenotype, assay, physical interaction
-
Reactome Reaction:
BAD
→
AKT1
(reaction)
Khor et al., Cancer Lett 2004*, Guo et al., Oncogene 2010*, Datta et al., Cell 1997*, del Peso et al., Science 1997*
-
WikiPathways Focal Adhesion-PI3K-Akt-mTOR-signaling pathway:
AKT1/AKT3/AKT2
→
BAD
(inhibition)
-
WikiPathways PI3K-AKT-mTOR signaling pathway and therapeutic opportunities:
AKT1
→
FOXO3/FOXO1/BAD/CDKN1B/GSK3B/FOXO4
(activation)
-
WikiPathways Rac1/Pak1/p38/MMP-2 pathway:
AKT1
→
BAD
(activation)
-
WikiPathways Apoptosis:
AKT1
→
BAD
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
BAD
—
AKT1
(direct interaction, enzymatic study)
Deregibus et al., J Biol Chem 2002*
-
IRef Biogrid Interaction:
BAD
—
AKT1
(physical association, affinity chromatography technology)
Song et al., J Cell Biol 2005*
-
IRef Biogrid Interaction:
BAD
—
AKT1
(direct interaction, enzymatic study)
Song et al., J Cell Biol 2005*
-
IRef Biogrid Interaction:
BAD
—
AKT1
(direct interaction, enzymatic study)
Polzien et al., J Biol Chem 2009*
-
IRef Biogrid Interaction:
BAD
—
AKT1
(direct interaction, pull down)
Wang et al., EMBO J 2001
-
IRef Innatedb Interaction:
BAD
—
AKT1
(unknown, -)
Song et al., J Cell Biol 2005*
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