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AKT increases the amount of BCL2. 127 / 130
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"Akt also has been reported to stimulate the expression of anti-apoptotic Bcl-2 proteins, such as Bcl-xL through the activation of NF-kappaB [XREF_BIBR, XREF_BIBR]."

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"Akt regulation of ERalpha on a post-translational level, may lead to increased Bcl-2 expression."

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"MIF [XREF_BIBR], an ERK activator inducing Bcl-2 expression, and AKT, or PKCepsilon [XREF_BIBR], responsible for MAPK activation, are both reported to be involved in the modulation of apoptosis in SSc fibroblasts."

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"107 PI-3K/Akt survival signaling modulates Bcl-2 expression via NF-kB and phosphorylating the anti-apoptotic proteins Bad and XIAP."

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"Moreover, when Akt was directly activated by its activator SC79 in DEX induced BMSCs, the activated Akt up-regulated the Bcl-2 protein level, as well as inducing a synergistic effect of cleaved-caspase-3 down-regulation."

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"AKT potentiates Bcl-2 expression through ERalpha."

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"FGF2 then acts extracellularly to activate the AKT and ERK signaling pathway which in turn increases BCL-2 expression, leading to inhibition of caspase-3 activity, thereby promoting cell survival."

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"This suggests that although AKT inhibition can inhibit expression of anti-apoptotic bcl-2, the cells may attempt to counteract this by increasing Mcl-1 expression as a possible cellular compensatory mechanism."

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"Akt can regulate gene expression at the transcription level XREF_BIBR and increases the expression of Bcl-2 in PC12 cells and BAF/3 cells."

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"In addition, AKT increases the phosphorylated to total protein levels of BAD and BAX, as well as Bcl2 levels and mTORC1 activity promoting anti-apoptotic and anti-autophagic actions that support cell survival."

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"Perifosine, an Akt kinase inhibitor, reversed the decrease of Bax and caspase 3, 8, and 9, and reduced the protein level of p-Akt and Bcl2 in treated mice compared with in mice treated with Con A + ghrelin only (XREF_FIG)."

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"Activation of the AKT signaling can promote DC maturation by enhancing Bcl-2 expression and NF-kB activation [XREF_BIBR, XREF_BIBR], and is necessary for hexokinase II (HK-II) activation and subsequent glycolysis."

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"Akt and protein kinase B up-regulates Bcl-2 expression through cAMP response element binding protein."

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"Mechanistically, isoflurane promoted PI3K and AKT activation, upregulated B-cell lymphoma2 (Bcl-2)-associated X protein and Bcl-2 expression levels, and reduced the expression levels of caspase-3 and caspase-8 in myocardial cells."

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"We observed that COL11A1 and Akt Ser473 / CREB Ser133 promotes BCL-2 levels and p-BAX Ser184 activity while decreasing BAX expression, which suppresses formation of the BAX and BAX homodimer, BAX and VDAC heterodimer and BAX, ANT, and VDAC complex, deactivating MPTP function, increasing Deltapsi m and decreasing MOMP, blocking leakage of Cyt-C into the cytosol and the combination of the Apaf-1, procaspase-9, and Cyt-C complex."

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"AKT also promotes leukemia T cells by enhancing the transcription of Bcl-2."

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"Activation of the PI3K and Akt pathway leads to increase the expression of Bcl-2 with the decrease the expression of Bax; therefore we assessed the effect of BBR on Bcl-2 and Bax proteins."

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"Activation of PI3K and Akt signaling enhances anti-apoptotic Bcl-2 protein expression and protects cells against apoptosis XREF_BIBR XREF_BIBR."

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"Akt also induces the expression of the anti-apoptotic Bcl-2 and c-FLIP proteins, and suppresses the cell cycle inhibitor p27 KIP [XREF_BIBR - XREF_BIBR]."

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"Furthermore, SIS gel protected cardiomyocytes from apoptosis by activating AKT and ERK pathways, and markedly up-regulated anti-apoptotic Bcl-2 expression but inhibited that of pro apoptotic Bax and c-caspase 3."

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"The PI3K pathway also regulates the expression of these proteins, as PI3K and Akt stimulates the expression of anti-apoptotic Bcl-2 proteins, such as Bcl-xL and Mcl-1, through the activation of NF-kB."

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"These observations are consistent with previous studies showing that inhibition of the PI3K and Akt pathway reduced p-Bad and Bcl-2 expression and induced ovarian cancer cell apoptosis in vitro XREF_BIBR, XREF_BIBR."

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"Pugazhenthi et al. reported that estrogens regulate the activation of Akt and PKB pathways, which induce the expression of BCL-2 mRNA through the phosphorylation of the cAMP response element (CRE) binding (CREB) protein and its subsequent binding to the CRE in the BCL-2 promoter [XREF_BIBR]."

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"Moreover, TRAF6 regulating cell apoptosis and invasive ability of gastric cancer cells might be associated with Akt activation and alterations of protein expression of Bcl2, Bax and MMP9."

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"Inhibition of AKT signaling can decrease protein expression of the anti-apoptotic BCL2 family member MCL1, via both GSK3 dependent and mTOR dependent pathways, XREF_BIBR, XREF_BIBR leading us to investigate whether MCL1 protein downregulation might mediate apoptosis induction following treatment with MYC and AKT pathway inhibitors."

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"Akt has also been reported to stimulate the expression of anti-apoptotic Bcl-2 proteins, such as Bcl-xL that prevents permeablization of the mitochondrial membrane by inhibiting activation of Bax and Bak [XREF_BIBR]."

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"XREF_BIBR reported that Akt and protein kinase B upregulates Bcl-2 expression through cAMP response element binding protein."

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"Akt upregulates the expression of Bcl-2 and thus leads to cell survival by phosphorylating and inhibiting proapoptotic proteins such as Bax [XREF_BIBR, XREF_BIBR, XREF_BIBR]."

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"Finally, CCK-8 and flow cytometry were used to detect the proliferation and apoptosis of differently treated cells, and the expression changes of proliferation and apoptosis marker proteins (AKT, p-AKT, caspase-3, BCL-2) were detected by Western blot."

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"Furthermore, Bax, a proapoptotic member of the Bcl-2 family, was found to be upregulated in leukemic cell lines treated with greensporone A. Interestingly, gene silencing of AKT using AKT specific siRNA suppressed the expression of Bcl-2 with enhanced expression of Bax."

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"In addition, the inhibition of mTOR and Akt might enhance the increased expression of Bax and decreases the expression of Bcl2 protein."

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"Akt can also upregulate Bcl-2 expression through cAMP response element binding protein."

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"Additionally, we demonstrated that blockade of PI3K and AKT signaling pathway by wortmannin (WM) impaired the expression of Bcl-2 and Bcl XL in the primary AML cells, suggesting an essential cross-talk between PI3K and Bcl-2 that maintains the survival of AML cells."

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"To examine whether PI3K and Akt signaling contributes to the expression of Bcl2 in H/R injury, we measured the mRNA level of Bcl2 by RT-PCR (XREF_FIG), as Bcl2 correlates with activation of cell survival signaling."

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"Meanwhile, Bcl-2 has strong antioxidant activity, and PI3K and AKT and ERK can up-regulate the expression level of Bcl-2 to inhibit ROS generation in ischaemic damage XREF_BIBR XREF_BIBR XREF_BIBR."

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"Meanwhile, Bcl-2 has strong antioxidant activity, and PI3K and AKT and ERK can up-regulate the expression level of Bcl-2 to inhibit ROS generation in ischemic damage [XREF_BIBR, XREF_BIBR]."

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"TxA2 activates the transcriptional factor CREB through both ERK and PI3K and AKT pathways, which may also lead to PCNA and Bcl-2 overexpressions and cell proliferation [XREF_BIBR]."

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"Our previous study suggested that enhanced AKT activation contributed to anti-apoptosis and cell growth by enhancing Bcl-2 expression and reducing Bax expression in SCK R cells, while enhanced ERK act[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"AKT is known to promote cell survival by upregulating the expression of BCL2 and downregulating the expression of BAX."

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"However, the Akt kinase inhibitor reversed the decrease of Bax and caspase 3, 8, 9, and reduced the protein level of p-Akt and Bcl-2."

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"Besides genetic alterations, aberrant Bcl-2 expression may also be caused by oncogenic activation of survival pathways, e.g., PI3K and Akt signaling."

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"Blockage of PI3K and Akt pathway with wortmannin also seriously impaired the protective effect of fibroblasts on myoblasts and fibroblast induced Bcl2 expression."

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"In rat pheochromocytoma (PC12) cells, Akt upregulates Bcl-2 expression through the c-AMP response element binding protein [16], but any effect on Bcl-x L has not been addressed."

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"Furthermore, AKT -inhibitor increased the expression of BAX and Caspase3, and inhibited the expression of p-AKT, AKT, p-mTOR, mTOR, BCL2, PSMD9, p-CDK1, CDK1, p-CCNB1 and CCNB1 in EECs."

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"NNM-25 inhibited the PARP-1 activity, AKT phosphorylation, up-regulated the protein expression of p53, Bad, and mTOR as well as down-regulating the protein expression of Bcl-2 and decreasing mitochondrial membrane potential."

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"This results, in part, in activation of PI3K-Akt signaling pathway, which mediates signaling of neuronal survival as well as enhanced expression of anti-apoptotic Bcl2 and Bcl-xl."

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"8 Furthermore, AKT induced up-regulation of BCL2 expression through cAMP response element binding protein has been reported."

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"Akt upregulates Bcl-2 and Mcl-1 expression via the cyclic adenosine monophosphate response element binding protein (CREB)."

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"360 Direct phosphorylation of CREB by AKT further promotes cell survival, possibly in part by inducing the expression of Bcl-2."

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"The ER is required for potentiation of Bcl-2 expression by AKT."

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"A possible mechanism for this protective effect was further explored and we believe that Reg3beta stimulates Akt phosphorylation which in turn increases Bcl-2 and Bcl-xL levels, key factors in stabilizing the integrity of mitochondria and cell survival."

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"IL-2 induces cell death via Stat2 mediated induction of the death receptor ligand Fas, whereas IL-2 promotes cell survival via Akt mediated induction of Bcl-2 expression."

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"Combined inhibition of Aurora A and AKT down-regulated the expression of Bcl-2/Bax and up-regulated the expression of cleaved-caspase-3 and cleaved-PARP."

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"Activation of PI3K and AKT pathway targeting ER-Ser167 and regulation of Bcl-2 expression in response to FGF7 treatment were identified to underlie FGFR2 dependent resistance to tamoxifen."

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"In ECs, VEGFA-induced cell survival depends on Flk-1/KDR and on the consequent activation of PI3K and Akt, which induces A1 and Bcl-2 expression [50]."

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"Akt also activates the transcription factor NF-kB and induces expression of anti-apoptotic Bcl-2, FLIP and IAP proteins."

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"XREF_BIBR Although AKT inhibition by wortmannin in propofol treated cells decreased Bcl-2 protein expression and increased cell death, wortmannin treatment had no effects on propofol induced Bcl-2 gene expression."

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"miR-221 is involved in the pathogenesis of MI/RI by regulating the PTEN and AKT signaling pathway, along with Bax and Bcl2 expression."

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"In addition, AKT kinase up-regulates Bcl-2 expression with BCL-2 preventing apoptosis independent of the structure of the causing drug [XREF_BIBR]."

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"Both PI3K and AKT inhibition decreased BCL-2 expression and increased BAX expression without effect on MCL-1, BCL-X L or BAK (XREF_FIG)."

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"In addition, activation of Akt pathway in these Smad4 deficient and K-Ras activated CRC cell lines (XREF_FIG) and in the corresponding tumours (XREF_FIG) induced the expression of anti-apoptotic Bcl-2, Bcl-w, and Survivin and reduced pro apoptotic Bim that might be involved in the acquisition of resistance to 5-FU-based therapy."

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"Inhibition of AKT pathway decreases the expression of Bcl2 and XIAP proteins but not Bcl-XL protein in endometriotic epithelial cells and stromal cells."

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"Furthermore, the related protein level of PI3K/AKT signaling pathway was also reduced, which suggested that the alteration of ROS was regulated by PI3K/AKT pathway, which leads to the alteration of Bcl-2/Bax protein expression level (Fig. 4c, d, Additional file 1: Fig. S1C, D)."

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"Akt can upregulate the Bcl-2 expression and increase the GSH and SOD activity to inhibit ROS generation in neurons in ischemic insult (Gao et al., 2015; Jiao et al., 2016; Zhang et al., 2015)."

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"After 24 hr exposure to 0.5 mM METH, we observed a significant 28% up-regulation of this protein (XREF_FIG), Inhibition of the ERK and Akt pathways decreases Bcl-2 expression levels in the cells by 55% and 20% respectively."

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"Pugazhenthi et al. reported that estrogens regulate the activation of Akt and PKB pathways, which induce the expression of BCL-2 mRNA through the phosphorylation of the cAMP response element (CRE) binding (CREB) protein and its subsequent binding to the CRE in the BCL-2 promoter [XREF_BIBR]."

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"Furthermore, knockdown of Akt by small interfering (si) RNA significantly increased the expression of bax, cleaved caspase3 and reduced the expression of bcl2 and cyclinD1 in SKM-1 cells."

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"When Akt was inhibited by MK-2206 2HCl in DEX induced cells in the presence of PRP-Exos, the results demonstrated that treatment with PRP-Exos rescued Bcl-2 protein expression, which was blocked by the inhibition of Akt."

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"On the other hand, upregulation of the PI3K and Akt pathway could increase the relative expression level of Bcl-2 and decrease the relative expression levels of Bax and Bim, while inhibition of the PI3K and Akt pathway led to adverse results."

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"Expression of anti-apoptotic Bcl-2 proteins related to survival is induced by activation of PI3K and Akt signaling and the Bcl-2 and Bax ratio is a critical determinant for induction of apoptosis in n[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"It has been reported that Akt upregulates Bcl-2 expression whose promoter region contains a cAMP response element (CRE) site [XREF_BIBR - XREF_BIBR]."

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"Forkhead box O3a (FOXO3a) can be phosphorylated by Akt, and promotes cell apoptosis by either inducing expression of Bcl-2 family or upregulating the cell death receptor ligand FasL [XREF_BIBR]."

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"We also identified activation of PI3K and AKT signaling targeting ER-Ser167 and regulation of Bcl-2 expression as a mediator of FGFR2 promoted resistance to tamoxifen."

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"Moreover, blockade of Akt and survivin increased the expression of the pro apoptotic proteins Bax and caspase -3 and reduced the expression of the anti-apoptotic protein Bcl2."

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"Akt activation has also been shown to enhance expression of the anti-apoptotic gene bcl-2 through phosphorylation of cyclic AMP response binding protein (CREB) [XREF_BIBR]."

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"Moreover, PI3K and Akt signaling increases Bcl-2 levels and decreases Bax levels, promoting cell survival [XREF_BIBR]."
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"Akt elevates Bcl-2 expression via transcriptional regulation (64) and inhibits Bax translocation to mitochondria (65)."

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"The PI3K-Akt pathway promotes cell survival by phosphorylating the proapoptotic Bcl-2-associated death promotor (BAD) and up-regulating the expression of anti-apoptotic Bcl-2 and Bcl-xl [XREF_BIBR], inhibiting the caspase controlled intrinsic apoptotic pathway [XREF_BIBR]."

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"More importantly, activated PI3K promotes Akt phosphorylation, which increases Bcl-2 expression to down-regulate cardiomyocyte apoptotic activity XREF_BIBR."

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"AKT and GRIP-1 cooperatively enhance Bcl-2 expression."

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"However, unlike the observation that Akt upregulates Bcl-2 expression in BAF/3 cells (Ahmed et al. 1997), Akt promotes HMN1 cell survival in the absence of altering Bcl-2, Bcl-X, and Bax expression, which is consistent with data from hippocampal H19-7 neuronal cells and epithelial BRK cells (Eves et al. 1998; Sabbatini and McCormick 1999)."

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"The activation of SLAMF5 initiates Akt signaling cascade that increases the anti-apoptotic Bcl-2 gene expression and consequently enhances CLL cell survival."

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"Results show that Akt inhibition downregulates BCL2 expression, but upregulates caspase-3 expression compared to solvent controls (XREF_FIG C, 4D)."

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"Therefore, Akt and ERK activation may activate CREB and enhance Bcl-2 expression, thus attenuating apoptosis."

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"XREF_BIBR, XREF_BIBR, XREF_BIBR A previous study reported that AKT and mTOR pathway activation increased the expression of anti-apoptotic proteins Bcl-2 and Bcl-xL, resulting in cell survival and growth."

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"The transcription of Bcl-2 can be activated by Akt while sustained levels of Mcl-1 and c-FLIP come from the inhibitory effect of Akt on protein degradation [11,44]."

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"AKT activation induces expression of the anti-apoptotic Bcl-2, activation of NFkB, inhibition of Forkhead family of transcription factors, and inactivation of pro apoptotic Bad [22-25]."

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"Available data from previous literature reveal that activation of Akt up-regulates the expression of anti-apoptotic Bcl-2 through cAMP-response Element-binding protein (CREB) [36]."

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"Finally, AKT and GRIP1 cooperated to increase Bcl-2 protein expression to a greater level than either factor alone."

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"Activation of gp120-primed DC reduced the expression of Bcl2 and activated Akt, and the induction of cell apoptosis is ASK1-dependent."

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"Akt mediates VEGF-C-induced Bcl-2 expression in lymphatic endothelial cells."

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"Previous studies have shown [XREF_BIBR, XREF_BIBR] that inhibition of PI3K or AKT decreases the level of the antiapoptotic protein Bcl-2 and increases the level of the proapoptotic protein BAX."

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"The subsequent activation of the Akt pathway increased Bcl2 expression and decreased Bax expression."

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"Accordingly, Akt mediated phosphorylation is crucial for the capability of SATB1 to repress Nanog expression and to activate transcription of Bcl2 and Nestin genes."

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"The underlying mechanism of Reg3beta mediated protection seems to involve Akt activation which upregulates Bcl-2 and Bcl-xL levels and consequently promotes cell survival."

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"In addition, the suppression of AKT both ritonavir treatment and AKT siRNA decreased the expression of anti-apoptotic Bcl-2 expression."

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"For example, activation of the PI3K and Akt pathway following integrin receptor engagement induces expression of the anti-apoptotic protein Bcl-2 thereby enhancing cell survival."

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"The neuroprotective effects of flavonoids have been linked to activation of pro survival signaling mediated by the PI3 and Akt and Erk pathways that stimulate expression of the proto-typical anti-apoptotic genes Bcl-2 and XIAP XREF_BIBR - XREF_BIBR."

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"Thus, the expression levels of p53 and BCL-2 were mediated by the activated AKT kinase."

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"Meanwhile, we found that PI3k and Akt pathway was activated probably through DJ-1 directly binding to and negatively regulating PTEN, consequently resulting in Nrf2 phosphorylation and activation, and thereby inducing Nrf2 dependent P-glycoprotein (P-gp) and Bcl-2 expressions in the DJ-1-mediated MDR of SGC7901 gastric cancer cells."

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"The expression of MMP2, MMP9, Bcl2, Bax, cleaved caspase3, PTEN, p-PI3K, p-AKT, PI3K and AKT was detected by Western blot."

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"Activation of Akt stimulates expression of Bcl-2 and inhibits the expression of Bad, thus inhibiting the execution of apoptosis."

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"P-AKT could significantly up-regulate the expression of Bcl-2, and down-regulate the expression of Bax, but not alter the expression of PTEN in gastric cancer cells."

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"AKT activation increases the expression of the Bcl-2 through phosphorylation of cyclic AMP response binding protein."

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"In addition, the protein expression of NF-kappaB p65 and Nrf2 in cytoplasm and nucleus, AKT, p-AKT, Bcl-2 Bax and Caspase 3 were analyzed for further verification."

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"Similarly, TLR4 is implicated in protection against hyperoxia-induced ALI by promoting the expression of Bcl-2 and Phospho Akt (anti apoptotic factors) [81]."

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"PI3K and AKT activation may promote BCL-2 expression in reticulophagy and may play a protective role during the early stages of NAFLD development."

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"The Akt protein complex is involved in the neuron structure, cell survival, and cell death through apoptosis and also stimulates the expression of Bcl-2, thereby inhibiting apoptosis (Lawlor and Alessi 2001; Huang and Reichardt 2003)."

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"Moreover, inhibition of PI3K and Akt signaling diminished p-p53 and caspase-3 levels, but increased BCL2 expression."

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"AKT mediated activation of mammalian target of Rapamycin (mTOR) and inhibition of glycogen synthase kinase (GSK3) promote hypertrophy by stimulating protein synthesis; AKT mediated phosphorylation of FOXO (Forkhead box containing protein, O-subfamily) contributes to the hypertrophic effect, by inhibiting the activation of E3-ubiquitin ligases, which trigger protein degradation; AKT dependent activation of Bcl2 and p21 expression supports the survival effect of IGF1."

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"The Akt activation enhances the expression of Bcl-2 anti-apoptotic gene via phosphorylation of cyclic AMP response binding protein (Pugazhenthi et al., 2000)."

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"25 Akt also activates the expression of the antiapoptotic gene Bcl-2, which negatively controls the expression of proapoptotic gene Bax, XREF_BIBR, XREF_BIBR and subsequently inhibits the mitochondria induced apoptotic signaling cascade."

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"Indeed, knockdown of Akt, CREB, or ATF1 in t-Darpp-expressing cells reduced Bcl2 protein levels."

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"The activation of the PI3k and Akt pathway can induce Bcl-2 expression in vascular endothelial cells."

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"Mechanistically, isoflurane promoted PI3K/AKT activation, upregulated B-cell lymphoma 2 (Bcl-2)-associated X protein and Bcl-2 expression levels, and reduced the expression levels of caspase-3 and caspase-8 in myocardial cells."

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"It has been reported that Akt activation leads to the overexpression of Bcl-2 and nicotine can activate Akt via PI3 kinase thereby inducing Bcl-2 and Bcl-x upregulation."

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"Akt activation has also been shown to enhance expression of the anti-apoptotic gene bcl-2 through phosphorylation of cylic AMP response binding protein (CREB) [XREF_BIBR]."

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"PECAM-1 dependent PI3K and Akt pathway activation has been shown to upregulate expression of anti-apoptotic Bcl-2 family proteins (including Bcl-xL and Bcl-2), thus preventing the intrinsic apoptosis [XREF_BIBR, XREF_BIBR]."

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"ARTN activation of AKT was previously demonstrated to promote the expression of BCL-2 and TWIST1 resulting in enhanced oncogenicity and an increased CSC population in breast cancer [XREF_BIBR, XREF_BIBR]."

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"PI-3K/Akt survival signaling modulates Bcl-2 expression via NF-kB and phosphorylating the anti-apoptotic proteins Bad and XIAP."

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"Further study revealed that activation of PERK-eIF2alpha induced the expression of transcription factor CHOP, which subsequently promoted apoptosis by downregulating BCL-2/MCL-1, promoting JNK signaling and suppressing AKT signaling."

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"Considering the expression variances of Bcl-2 and Mcl-1 in PEO4 cells, it is possible that the increased Mcl-1 expression was induced by the loss of Bcl-2 expression in response to AKT inhibition, utilizing as a potential compensatory mechanism."

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"Levels of Bcl-2 were elevated in AGEs- and high glucose treated cells, and were attenuated by inhibitors of PI3-kinase, Akt and NF-kappaB."

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"Here, we show that ERalpha, both AF-I and AF-II domains, is targeted by AKT to bring about potentiation of Bcl-2 expression at both the transcriptional and translational levels (XREF_FIG and XREF_FIG)."

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"Through receptor signaling, FGF2 activated the AKT and ERK signaling pathways, which in turn increased BCL-2 expression."

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"XREF_BIBR The activation of the PI3K and Akt signaling can induce antiapoptotic Bcl-2 expression and inhibit pro apoptotic Bax expression and caspase activation."

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"It has been indicated that Akt activation induced expression of the anti-apoptotic Bcl-2 (Akca et al., 2011)."