IndraLab
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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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"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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"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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"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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"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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"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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"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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"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."