◀ Back to AKT2
AKT2 — CHUK
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
CHUK
→
AKT2
(directlyIncreases, CHUK Activity)
Yuan et al., J Biol Chem 2002*
Evidence: TNFalpha-induced AKT2 and constitutively active AKT2 phosphorylated IKKalpha (Fig. 4B) but not NIK (data not shown)
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OpenBEL Selventa BEL large corpus:
CHUK
→
AKT2
(directlyIncreases, CHUK Activity)
Yuan et al., J Biol Chem 2002*
Evidence: As shown in Fig. 4C, IKKalpha was highly phosphorylated in cells expressing constitutively active AKT2 but not in the cells transfected with pcDNA3 and dominant-negative AKT2. Collectively, these data indicate that IKKalpha is an AKT2 physiological substrate.
-
OpenBEL Selventa BEL large corpus:
CHUK
→
AKT2
(directlyIncreases, CHUK Activity)
Yuan et al., J Biol Chem 2002*
Evidence: AKT2 interacts with and phosphorylates I kappa B kinase alpha ()
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KEGG Apoptosis:
AKT1/AKT2/AKT3
→
CHUK/IKBKB/IKBKG
(protein-protein, activation)
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KEGG B cell receptor signaling pathway:
AKT1/AKT2/AKT3
→
Complex of CHUK-IKBKB-IKBKG
(protein-protein, phosphorylation)
-
KEGG Pathways in cancer:
AKT1/AKT2/AKT3
→
CHUK/IKBKB/IKBKG
(protein-protein, activation)
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KEGG Pancreatic cancer:
AKT1/AKT2/AKT3
→
CHUK/IKBKB/IKBKG
(protein-protein, activation)
-
KEGG Prostate cancer:
AKT1/AKT2/AKT3
→
CHUK/IKBKB/IKBKG
(protein-protein, activation)
-
KEGG Chronic myeloid leukemia:
AKT1/AKT2/AKT3
→
CHUK/IKBKB/IKBKG
(protein-protein, activation)
-
KEGG Acute myeloid leukemia:
AKT1/AKT2/AKT3
→
CHUK/IKBKB/IKBKG
(protein-protein, activation)
-
KEGG Small cell lung cancer:
AKT1/AKT2/AKT3
→
CHUK/IKBKB/IKBKG
(protein-protein, activation)
-
KEGG Chemokine signaling pathway:
AKT1/AKT2/AKT3
→
CHUK/IKBKB/IKBKG
(protein-protein, phosphorylation)
-
WikiPathways Chemokine signaling pathway:
AKT1/AKT2/AKT3
→
CHUK/IKBKB/IKBKG
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
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IRef Bind_translation Interaction:
CHUK
—
AKT2
(experimental interaction detection)
Yuan et al., J Biol Chem 2002*
-
IRef Bind_translation Interaction:
CHUK
—
AKT2
(coimmunoprecipitation)
Yuan et al., J Biol Chem 2002*
-
IRef Biogrid Interaction:
CHUK
—
AKT2
(physical association, affinity chromatography technology)
Barré et al., EMBO J 2007
-
IRef Biogrid Interaction:
CHUK
—
AKT2
(physical association, affinity chromatography technology)
Yuan et al., J Biol Chem 2002*
-
IRef Biogrid Interaction:
CHUK
—
AKT2
(direct interaction, enzymatic study)
Yuan et al., J Biol Chem 2002*
-
IRef Hprd Interaction:
CHUK
—
AKT2
(in vivo)
Yuan et al., J Biol Chem 2002*
-
IRef Hprd Interaction:
CHUK
—
AKT2
(in vitro)
Yuan et al., J Biol Chem 2002*
-
IRef Innatedb Interaction:
CHUK
—
AKT2
(unknown, -)
Yuan et al., J Biol Chem 2002*
-
IRef Ophid Interaction:
CHUK
—
AKT2
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Ozes et al., Nature 1999
:
Akt mediates
IKKalpha phosphorylation at threonine 23
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
Saleem et al., Oncogene 2004
(Edema...) :
We found that Lupeol treatment to mouse skin resulted in the inhibition of TPA induced ( i ) activation of PI3K, ( ii ) phosphorylation of
Akt at Thr ( 308 ), ( iii )
activation of NF-kappaB and
IKKalpha , and ( iv ) degradation and phosphorylation of IkappaBalpha
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
Gustin et al., J Biol Chem 2006
:
This study shows that
Akt binds to and
increases the activity of
IKKalpha and thereby increases p52 production in cells
Dan et al., Cancer Res 2007
(Prostatic Neoplasms) :
Additionally,
IKKalpha is
required for efficient induction of mTOR activity downstream of constitutively active
Akt expression
Yeh et al., Biochem Pharmacol 2008
(Chondrosarcoma) :
The TGF-beta1 mediated increases in
IKKalpha/beta phosphorylation and p65 Ser ( 536 ) phosphorylation were
inhibited by Ly294002 and
Akt inhibitor
Otipoby et al., Proc Natl Acad Sci U S A 2008
:
BAFF activates
Akt and Erk through BAFF-R in an
IKK1 dependent manner in primary mouse B cells
Fong et al., Lung Cancer 2009
(Adenocarcinoma...) :
The OPN mediated increases in
IKK alpha/beta , IkappaBalpha and p65 Ser ( 536 ) phosphorylation were
inhibited by Ly294002,
Akt inhibitor and PD98059
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