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BCL-xL promotes cell survival by binding BH3-only initiators through its hydrophobic groove. Combining resonance energy transfer assays and molecular dynamics simulations, we unravel that membrane anchoring of BCL-xL via its C-terminal tail selectively advantages binding to membrane-anchored PUMA in...
ORGANISM(S): Homo sapiens (Human) 
2025-12-08 | PXD066303 | Pride
Putting the STING back into BH3-mimetic drugs for TP53 mutant blood cancers
Intrinsic apoptosis is principally regulated by the BCL-2 family of proteins, but some non-BCL-2 proteins also serve as important regulators. To identify novel apoptosis regulators, we performed a genome-wide CRISPR-Cas9 library screen, and it identified the mitochondrial E3 ubiquitin ligase MARCHF5...
ORGANISM(S): Mus musculus (Mouse) 
2022-09-25 | PXD030246 | Pride
TP53-mutant blood cancers remain a major clinical challenge. BH3-mimetic drugs inhibit BCL-2 pro-survival proteins to promote cancer cell apoptosis. Despite acting downstream of TP53, functional TP53 is required for maximal cancer cell killing by BH3-mimetics through an unknown mechanism. Here, we r...
ORGANISM(S): Mus musculus 
2024-04-25 | GSE261373 | GEO
Overexpression of antiapoptotic BCL2 family proteins occurs in various hematologic malignanices and contributes to leukemogenesis by inhibiting the apoptotic machinery of the cells. BH3 mimetics provide an option for medication, with venetoclax as the first drug applied for chronic lymphocytic leuke...
ORGANISM(S): Homo sapiens 
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