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HSPA6 is a cigarette smoke-induced ulcerative colitis (UC)-susceptibility gene. The HSPA6 risk locus is associated with decreased HSPA6 expression. HSPA6 provides epithelial protection by stabilizing anti-apoptotic Bcl-XL, thereby contributing to the beneficial effect of cigarette smoking in UC.
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our findings identify let-7b as a key regulator in platelet apoptosis by demonstrating let-7b targeting of Bcl-xL. Increasing let-7b expression during storage downregulates expression of antiapoptotic Bcl-xL and ultimately frees Bak to induce platelet apoptosis.
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The inhibition of MCL-1, BCL-XL, and FGFR1 to maximize therapeutic response in FGFR1-expressing lung SqCC.
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Examined the roles of BCL2 proteins in the induction of apoptosis in cells upon infection with flaviviruses, such as Japanese encephalitis virus, Dengue virus and Zika virus. Showed that survival of the infected cells depends on BCLXL, a pro-survival BCL2 protein due to suppression of the expression of another pro-survival protein, MCL1.
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Bcl-xL abrogates the cytotoxic effects of LRRK2 inhibition in a neuroblastoma cell line (SH-SY5Y/Bcl-xL) overexpressing Bcl-xL.
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E2F1 interacts with BCL-xL independently from its BH3 binding interface and induces a stabilization of BCL-xL at mitochondrial membranes. This prevents efficient control of BCL-xL over its binding partners, in particular over BAK resulting in the induction of cell death.
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Study shows that multiple ion transporters mediate the rise in pH that increases the rate of Bcl-xL deamidation in response to DNA damage in certain cells. Additionally, deamidation of Bcl-xL is intramolecularly catalyzed in a manner that is dependent upon two conserved histidines near each of the deamidation sites and that they may function together as a pH-sensitive switch.
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hTERT contains a BH3-like motif, a short peptide sequence found in BCL-2 family proteins, and interacts with anti-apoptotic BCL-2 family proteins MCL-1 and BCL-xL
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Study demonstrated that lncRNA-HEIH regulates miR-939 expression through transcriptional repression of Bcl-xL promoting colorectal tumorigenesis.
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Results showed that the expressions of RIP2 and BclxL were positively correlated with the malignant grade of astrocytoma. RIP2 promoted human glioblastoma cell proliferation by inducing expression of BclxL.
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BCL-XL has a role in modulating RAS signalling to favor breast cancer cell stemness
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Bcl-xL degradation during endoplasmic reticulum stress-induced apoptosis is mediated by RNF183.RNF183 ubiquitinates Bcl-xL.
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BCL-XL promotes stemness and contributes to the aggressiveness of both melanoma and glioblastoma.
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inhibition of the BCL2 family member BCLxL resulted in nanomolar potency against human synovial sarcoma cell lines and 50% tumor reduction in a genetically engineered mouse model
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In this study, we investigated whether APG-1252-12A inhibits the growth of five leukemia cell lines in a concentration- or time-dependent manner by MTS assay.APG-1252-12A is a Bcl-2 homology (BH)-3 mimetic that specifically binds to Bcl-2 and Bcl-xl, which has shown efficacy in some Bcl-2 dependent hematological cancers
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inhibition of Bcl-xL induces significantly more apoptosis in IDH1-mutated cells than in wild-type IDH1 cells.
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CCAT1 is upregulated in docetaxel-resistant lung adenocarcinoma cells; its oncogenic function depends on sponging of let-7c, which releases Bcl-xl, promoting the acquisition of chemoresistance and epithelial-to-mesenchymal transition phenotypes
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In the epithelial ovarian cancer stem cells, 40% knock-down of Bclxl expression was sufficient to induce the full activation of caspases. Bclxl expression levels in EOC cells is dynamic and can be regulated by microenvironments that are enriched with the pro-inflammatory cytokine IL-6 such as the cancer stem cell and adipocyte niches.
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Study reports the interaction of BCL-XL with RASSF6. BCL-XL inhibits the interaction between RASSF6 and MDM2 and suppresses p53 expression. Consequently, BCL-XL antagonizes RASSF6-mediated apoptosis. Thus, the inhibition of RASSF6-mediated apoptosis also underlies the prosurvival role of BCL-XL.
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anti-apoptotic molecules BclxL and Bcl-2 and the pro-apoptotic factors BAD and BID cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L.
