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AKT1 — PIK3CB
Pathways - manually collected, often from reviews:
-
KEGG Apoptosis:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, indirect effect)
-
KEGG VEGF signaling pathway:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Osteoclast differentiation:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, activation)
-
KEGG Focal adhesion:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Jak-STAT signaling pathway:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, phosphorylation)
-
KEGG T cell receptor signaling pathway:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG B cell receptor signaling pathway:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein)
-
KEGG Fc gamma R-mediated phagocytosis:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Neurotrophin signaling pathway:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Cholinergic synapse:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, activation)
-
KEGG Chagas disease (American trypanosomiasis):
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Measles:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Influenza A:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG ErbB signaling pathway:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Colorectal cancer:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, activation)
-
KEGG Renal cell carcinoma:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, indirect effect)
-
KEGG Prostate cancer:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Melanoma:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Chronic myeloid leukemia:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Acute myeloid leukemia:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Small cell lung cancer:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Non-small cell lung cancer:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Non-small cell lung cancer:
PIK3CA/PIK3CB/PIK3CD/PIK3CG
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
KEGG Chemokine signaling pathway:
PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3/PIK3R5
→
AKT1/AKT2/AKT3
(protein-protein, compound)
-
WikiPathways Regulation of toll-like receptor signaling pathway:
PIK3R5/PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3
→
AKT3/AKT1/AKT2
(activation)
-
WikiPathways Toll-like Receptor Signaling Pathway:
PIK3R5/PIK3CA/PIK3CB/PIK3CD/PIK3CG/PIK3R1/PIK3R2/PIK3R3
→
AKT3/AKT1/AKT2
(activation)
-
WikiPathways AMP-activated Protein Kinase (AMPK) Signaling:
Complex of PIK3R3-PIK3R1-PIK3CB-PIK3CA-PIK3CG-PIK3CD-PIK3R2
→
AKT1
(activation)
-
WikiPathways Chemokine signaling pathway:
PIK3CA/PIK3CD/PIK3R1/PIK3R2/PIK3R3/PIK3CG/PIK3R5/PIK3CB
→
AKT1/AKT2/AKT3
(activation)
Text-mined interactions from Literome
Kubo et al., Biochem J 2005
:
Specific
role for
p85/p110beta in GTP-binding-protein mediated activation of
Akt
Komori et al., Clinical calcium 2006
:
Phosphoinositide 3-kinase
(PI3K)-Akt signaling enhances DNA binding of Runx2 and Runx2 dependent transcription, and Runx2
upregulates PI3K subunits ( p85 and
p110 beta ) and Akt
Torbett et al., Biochem J 2008
(Breast Neoplasms) :
In contrast,
p110beta-selective inhibitors only
reduced PKB/Akt phosphorylation in PTEN ( phosphatase and tensin homologue deleted on chromosome 10 ) mutant cell lines, and was associated with a lesser decrease in S6 phosphorylation ... In contrast,
p110beta-selective inhibitors only
reduced PKB/Akt phosphorylation in PTEN ( phosphatase and tensin homologue deleted on chromosome 10 ) mutant cell lines, and was associated with a lesser decrease in S6 phosphorylation
Guillermet-Guibert et al., Proc Natl Acad Sci U S A 2008
:
In macrophages, both
p110beta and p110gamma
contributed to
Akt activation induced by the GPCR agonist complement 5a, but not by the Tyr kinase ligand colony stimulating factor-1 ... In fibroblasts, which express p110beta but not p110gamma,
p110beta mediated
Akt activation by the GPCR ligands stromal cell derived factor, sphingosine-1-phosphate, and lysophosphatidic acid but not by the Tyr kinase ligands PDGF, insulin, and insulin-like growth factor 1
Canobbio et al., Blood 2009
:
However,
PI3Kbeta , but not PI3Kgamma, enzymatic activity was absolutely
required for
Akt phosphorylation, Rap1 activation, and platelet aggregation downstream of the immunoreceptor tyrosine based activation motif ( ITAM ) -bearing receptor glycoprotein VI (GPVI)
Kim et al., J Biol Chem 2009
:
In addition, GPVI induced Akt phosphorylation in the presence of ADP antagonists was completely inhibited by PI3K inhibitor LY294002 and PI3Kbeta inhibitor TGX-221 indicating an essential
role of
PI3Kbeta in
Akt activation directly downstream of GPVI ... In addition, a significant portion of GPVI dependent, ADP independent Akt activation also exists, and
PI3Kbeta plays an essential role in GPVI mediated platelet aggregation and
Akt activation
Matheny et al., Cell Death Differ 2010
:
However, inhibition of
p110 beta catalytic activity did not
increase IGF-I stimulated
Akt activity, suggesting a role for p110 beta protein interactions rather than decreased generation of phosphoinositides in this effect
Ciraolo et al., Mol Biol Cell 2010
(Azoospermia...) :
In particular, p110beta is crucially needed in c-Kit mediated spermatogonial expansion, as c-Kit positive cells are lost in the adult testis and
activation of
Akt by SCF is blocked by a
p110beta inhibitor