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Overexpression of BCL-XL in human induced pluripotent stem cells (iPSC) provides highly efficient editing strategies and useful tools for applications ranging from manipulating human iPSC genomes to creating gene-modified animal models.
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In patients with oropharyngeal squamous cell carcinoma (OPSCC), combined bcl-2-like protein 1 apoptosis regulator (Bcl-xL) and tumor suppressor Protein p53 expression has a survival benefit in a select population of non-smokers with cyclin-dependent kinase inhibitor p16 positive disease. Smokers with a high Bcl-xL expression have an improved 5-year overall survival rate compared to those with low Bcl-xL expression.
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Variable BCL2/BCL2L1 ratio in multiple myeloma with t(11;14).
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post-translational modifications within the alpha1-alpha2 intrinsically disordered region promote its interaction with the folded core of Bcl-xL that inhibits the proapoptotic activity of two types of regulatory targets, BH3-only proteins and p53
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cytoplasmic apoptotic function of p73 is mediated through a noncanonical mode of Bcl-XL recognition
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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