◀ Back to AKT1
AKT1 — BCL10
Pathways - manually collected, often from reviews:
-
NCI Pathway Database BCR signaling pathway:
AKT1 (AKT1)
→
CARD11/BCL10/MALT1/TAK1 complex (CARD11-BCL10-MALT1-MAP3K7)
(modification, activates)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
AKT1
—
BCL10
(physical association, affinity chromatography technology)
Yeh et al., J Biol Chem 2006
-
IRef Biogrid Interaction:
AKT1
—
BCL10
(direct interaction, enzymatic study)
Yeh et al., J Biol Chem 2006
-
IRef Hprd Interaction:
AKT1
—
BCL10
(in vitro)
Yeh et al., J Biol Chem 2006
-
IRef Innatedb Interaction:
AKT1
—
BCL10
(unknown, -)
Yeh et al., J Biol Chem 2006
-
IRef Intact Interaction:
AKT1
—
BCL10
(physical association, anti bait coimmunoprecipitation)
Yeh et al., J Biol Chem 2006
-
IRef Intact Interaction:
AKT1
—
BCL10
(physical association, pull down)
Yeh et al., J Biol Chem 2006
-
IRef Intact Interaction:
AKT1
—
BCL10
(physical association, protein kinase assay)
Yeh et al., J Biol Chem 2006
Text-mined interactions from Literome
Jones et al., J Exp Med 2000
:
Protein kinase B regulates T lymphocyte survival, nuclear factor kappaB activation, and
Bcl-X ( L ) levels in vivo
Jost et al., J Biol Chem 2001
:
By using pharmacological inhibitors and dominant negative expression constructs, we observed that phosphatidylinositol
3-kinase/AKT and phospholipase C gamma/protein kinase C alpha activation were
required for keratinocyte survival independently of EGFR activation or
Bcl-x ( L ) expression
Porosnicu et al., Leukemia 2001
(Leukemia) :
Combined treatment with As2O3 and STI-571 also resulted in greater reductions in the levels of
Bcl-x ( L ), XIAP and Akt, and
inhibition of
Akt kinase activity
Sade et al., Eur J Immunol 2003
:
Thus, IL-7 regulates IAP-2 expression and
inhibits dexamethasone induced apoptosis by activating
Akt via PI3K dependent signaling, but regulates
Bcl-x ( L ) expression via a PI3K independent pathway in mature T cells
Versteeg et al., Circ Res 2004
:
In conclusion, our results show that FVIIa induces cell survival through STAT5 dependent
Bcl ( XL ) production and Jak2 dependent
activation of
PKB
Oh et al., Cell Death Differ 2006
:
DEX treatment upregulated cellular FLICE inhibitory protein ( cFLIP ) expression, but did not alter the protein levels of Bcl-2,
Bcl-xL , Mcl-1, and cIAP as well as
Akt activation
Narayan et al., Mol Cell Biol 2006
:
Finally, we provide evidence for a physical and functional interaction between Akt and CARMA and for
Akt dependent phosphorylation of
Bcl10
Bae et al., Cancer Res 2006
(Adenocarcinoma...) :
Bcl-w overexpression also
activated phosphoinositide 3-kinase (PI3K),
Akt , and Sp1, and the blocking effects of each of these components using pharmacologic inhibitors, dominant negative mutants, or small interfering RNA abolished the ability of Bcl-w to induce MMP-2 and cell invasion
Kozuma et al., Journal of thrombosis and haemostasis : JTH 2007
:
Continuous expression of
Bcl-xL protein during megakaryopoiesis is post-translationally
regulated by thrombopoietin mediated
Akt activation, which prevents the cleavage of Bcl-xL
Longo et al., Blood 2008
(Leukemia, Lymphocytic, Chronic, B-Cell...) :
Sustained activation of
Akt resulted in increased leukemic cell viability and increased expression of the antiapoptotic proteins Mcl-1,
Bcl-xL , and X-linked inhibitor of apoptosis protein ( XIAP ), thus largely recapitulating the effects of sustained BCR stimulation
Kuo et al., Blood 2008
(Lymphoma, B-Cell, Marginal Zone...) :
Inhibition of
AKT by LY294002 ( a PI3K inhibitor )
blocked BCL10 nuclear translocation, NF-kappaB transactivity, and BAFF expression ... In B-cell lymphoma Pfeiffer cells, BAFF activated NF-kappaB and AKT ; the activated NF-kappaB
up-regulated BCL10 , and the activated
AKT caused formation of BCL10/BCL3 complexes that translocated to the nucleus
Flacke et al., Apoptosis 2009
:
Acidic preconditioning protects endothelial cells against apoptosis through p38- and
Akt dependent
Bcl-xL overexpression
Garofalo et al., PloS one 2008
:
Our data provide evidence that
Bcl-w is a new member of the Akt pathway and that
Akt may
induce anti-apoptotic signals at least in part through the regulation of the amount and activity of Bcl-w
Wang et al., Cancer Lett 2010
(Ovarian Neoplasms) :
Meanwhile, the further study demonstrates that the chemoresistance caused by IL-6 is associated with increased expression of both multidrug resistance related genes ( MDR1 and GSTpi ) and apoptosis inhibitory proteins ( Bcl-2,
Bcl-xL and XIAP ), as well as
activation of Ras/MEK/ERK and
PI3K/Akt signaling
Deeb et al., Carcinogenesis 2011
(Adenocarcinoma...) :
Further,
Akt , NF-?B and NF-?B
regulated Bcl-2,
Bcl-xL , survivin and cIAP1 appear to be the molecular targets of CDDO for inhibiting the progression of prostate cancer in TRAMP mice
Zhao et al., J Lipid Res 2012
:
Further studies showed that TNF-a decreased expression of the antiapoptotic proteins Bcl-2 and
Bcl-xL , decreased I?Ba and PPAR?, and also
inhibited PI3K dependent
Akt and EGFR signaling
Jacquin et al., Cell Death Differ 2013
:
Active
Akt prevents FoxO nuclear localization, which precludes Bcl-6 expression and leads to
Bcl-xL overexpression