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AKT1 — BCL2
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Matsuzaki et al., J Neurochem 1999
:
Adenovirus mediated overexpression of the activated form of
Akt significantly
inhibited NO-induced cell death, caspase-3-like activation, and changes in
Bcl-2 and Bax expression
Campbell et al., J Biol Chem 2001
(Breast Neoplasms) :
Moreover,
AKT overexpression
led to up-regulation of estrogen regulated pS2 gene,
Bcl-2 , and macrophage inhibitory cytokine 1
Honda et al., J Neurosci Res 2001
(Alzheimer Disease...) :
Furthermore, 17beta-estradiol induced phosphorylation of the cAMP response element binding protein ( CREB ) at Ser ( 133 ) within 15 min and then upregulated
Bcl-2 in a
PI3-K/Akt dependent manner
Choi et al., Int J Oncol 2002
:
Bcl-2 overexpression
attenuates arsenic trioxide induced apoptosis in U937 cells by inhibition of caspase 3 activity, but not inhibition of
Akt
Fahy et al., Br J Cancer 2003
(Adenocarcinoma...) :
Inhibition of either phosphatidylinositol-3 kinase or
AKT led to a decreased protein level of the antiapoptotic gene
BCL-2 and an increased protein level of the proapoptotic gene BAX
Gagnon et al., Int J Oncol 2003
(Endometrial Neoplasms) :
Although, Bcl-2 expression was strongly expressed in mutated-PTEN cells, expression remained stable in the presence of Wortmannin suggesting that
Bcl-2 is not
regulated by
Akt
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
Asnaghi et al., Oncogene 2004
:
Bcl-2 phosphorylation and apoptosis activated by damaged microtubules require mTOR and are
regulated by
Akt
Asnaghi et al., Pharmacol Res 2004
:
We also found that the level of activity of
Akt can
regulate Bcl-2 phosphorylation, through the mTOR kinase
Hui et al., Brain Res 2005
(Brain Ischemia) :
In contrast, insulin, a PI3K agonist, not only obviously activated
Akt1 during early and later reperfusion, but also
inhibited phosphorylation of JNK1/2, c-Jun, and
Bcl-2 and attenuated the activation of caspase-3
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
Woo et al., Apoptosis 2005
:
In the present study, we determined the
effect of the anti-apoptosis protein
Bcl-2 on caspase-3 activation, PLC-gamma1 degradation and
Akt activation during the various anticancer agents induced apoptosis
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
Das et al., J Mol Cell Cardiol 2007
(Myocardial Reperfusion Injury) :
The survival signal was further confirmed by increased phosphorylation of
AKT and
enhanced induction of expression of
Bcl-2 during adaptation and its reversal with desipramine
Yasuhara et al., J Neurosci 2006
(Disease Models, Animal...) :
Administration of the HB1.F3 supernatant to human derived dopaminergic SH-SY5Y cells and fetal rat ventral mesencephalic dopaminergic neurons protected against 6-hydroxydopamine neurotoxicity by suppressing apoptosis through
Bcl-2 upregulation, which was
blocked by anti-stem cell factor antibody alone, the phosphatidylinositol
3-kinase/Akt inhibitor LY294002 [ 2- ( 4-morpholinyl ) -8-phenyl-1 ( 4H ) -benzopyran-4-one ] alone, or a combination of both
Poggi et al., Clin Dev Immunol 2006
(HIV Infections) :
TGF-beta enhances starvation induced NK cell apoptosis, reduces the transcription of the antiapoptotic protein
Bcl-2 and
inhibits Akt phosphorylation induced by oligomerization of the triggering NK cell receptor NKG2D
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
Moon et al., Toxicon 2008
:
Melittin
induces Bcl-2 and caspase-3 dependent apoptosis through downregulation of
Akt phosphorylation in human leukemic U937 cells
Lim et al., J Neurosci Res 2008
:
Thus, MAPK/ERK dependent p35 up-regulation and MAPK/ERK dependent and
PI3K/Akt dependent
Bcl2 up-regulation contribute to BDNF stimulated neural differentiation and to the survival of differentiated cells
Rochman et al., J Immunol 2008
(Lymphopenia) :
We now demonstrate that CD8 ( + ) T cells express TSLPR and that TSLP activates both STAT5 and
Akt and
induces Bcl-2 in these cells
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
Steinacker et al., Am J Pathol 2010
(Amyotrophic Lateral Sclerosis...) :
In the course of disease,
Bcl-2 decreases, nuclear factor-kappaB increases, and
Akt is
activated , but these changes were largely unaffected by Prp expression
Natalicchio et al., Endocrinology 2010
:
When cells were pretreated with exendin-4, TNFalpha induced JNK and IRS-1/2 serine phosphorylation was markedly reduced,
Akt phosphorylation was increased, caspase-3 and
Bcl-2 protein levels were
restored to normal, and TNFalpha induced apoptosis was inhibited by 50 %
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
Bratton et al., Int J Oncol 2010
(Breast Neoplasms) :
Regulation of ERalpha mediated transcription of
Bcl-2 by
PI3K-AKT crosstalk : implications for breast cancer cell survival
Rudner et al., Radiation oncology (London, England) 2010
(Carcinoma...) :
Akt activity and
regulation of the expression of
Bcl-2 family members and key downstream effectors involved in apoptosis regulation were examined by Western blot analysis
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 ... 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
Mou et al., Toxicol In Vitro 2011
(Carcinoma, Non-Small-Cell Lung) :
Furthermore, celastrol induced the release of cytochrome c. Celastrol also up-regulated the expression of pro-apoptotic Bax, down-regulated anti-apoptotic
Bcl-2 , and
inhibited Akt phosphorylation
Nishioka et al., Breast Cancer Res 2011
(Breast Neoplasms...) :
Our data also showed that
Akt functioned directly downstream of Src and was
responsible for the increase of
Bcl-2 expression and long-term cell survival
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 ... 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
Cassis et al., Kidney Int 2012
(Anemia...) :
Inhibition of
p-Akt by Wortmannin partially antagonized the effect of EPO on allograft injury and tubular apoptosis, and
prevented EPO induced
Bcl-2 upregulation
Guo et al., Zhonghua Xue Ye Xue Za Zhi 2012
(Precursor Cell Lymphoblastic Leukemia-Lymphoma) :
Oridonin inhibited activation of ABL kinase and its downstream
Akt/mTOR , Raf/MEK/ERK and STAT5 signaling pathways, which were constitutively activated in SUP-B15 cell line,
down-regulated the level of anti- apoptotic protein
Bcl-2 and up-regulated the expression of pro-apoptotic protein Bax
Liu et al., World J Gastroenterol 2012
(Reperfusion Injury) :
Compared with the GH group, expression of
Bcl-2 decreased and Bax increased in the D + GH, C + GH and L + GH groups, and
Akt decreased and GSK-3ß
increased in the L + GH group
Shukla et al., Neurotoxicology 2013
:
Sal toxicity coincided with reduced pAkt level and its downstream effectors : pCREB, pGSK-3ß,
Bcl-2 and neurotrophins GDNF, BDNF suggesting
repressed PI3K/Akt 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
Wang et al., J Chemother 2013
(Carcinoma, Non-Small-Cell Lung...) :
These data indicate that the cooperative effects of p-ERK1/2 and
p-Akt on attenuating cisplatin cytotoxicity are
mediated by PUMA and
Bcl-2 regulation, and concurrently blocking these pathways may be an effective strategy for improving the efficacy of cisplatin as anticancer treatment
Ahmed et al., Proc Natl Acad Sci U S A 1997
:
Expression of catalytically active
Akt mutants in BAF/3 cells expressing IL-2R beta [ A0 ] delta S
promotes the expression of
Bcl-2 and c-myc, inhibits apoptosis induced by IL-3 deprivation or staurosporine, and stimulates cell cycle progression