Ask about this productRelated genes to: Bcl-G antibody
- Gene:
- BCL2 NIH gene
- Name:
- BCL2 apoptosis regulator
- Previous symbol:
- -
- Synonyms:
- Bcl-2, PPP1R50
- Chromosome:
- 18q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2019-04-23
- Gene:
- BCL2L1 NIH gene
- Name:
- BCL2 like 1
- Previous symbol:
- -
- Synonyms:
- BCLX, BCL2L, Bcl-X, bcl-xL, bcl-xS, PPP1R52
- Chromosome:
- 20q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-30
- Date modifiied:
- 2016-01-13
- Gene:
- BCL9L NIH gene
- Name:
- BCL9 like
- Previous symbol:
- -
- Synonyms:
- DLNB11, B9L, Bcl9-2
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-09
- Date modifiied:
- 2018-11-16
Related products to: Bcl-G antibody
Related articles to: Bcl-G antibody
- Poly(ADP-ribose) polymerase (PARP) inhibitors (PARPis) induce regressions and extend progression-free survival (PFS) in ovarian cancer, especially in tumors with BRCA1 or BRCA2 mutations that impair homologous recombination repair. While recent studies have clarified the key roles of BRCA1, BRCA2, and PARP1 in replication fork stability, the downstream mechanisms that mediate PARPi-induced cytotoxicity and resistance remain incompletely understood. Here we delineate cell fate outcomes following PARPi treatment in homologous recombination-deficient high-grade serous ovarian cancer and identify actionable pathways to overcome acquired resistance. Our findings reveal that PARPi-induced DNA damage simultaneously triggers apoptosis, which primarily occurs through the BAX/BAK-dependent intrinsic apoptotic pathway, while also driving cellular senescence, as manifested by the expression of senescence-associated β-galactosidase, CDKN1A upregulation and a senescence-associated secretory phenotype. Notably, the PARPi-induced senescent cells persist as resistance develops and exhibit multinucleation, a hallmark of nuclear atypia, both in vitro and in patient-derived xenografts (PDXs). Building on the observation that the anti-apoptotic protein BCLX restrains pro-apoptotic BCL2 family members after PARPi treatment, we show that addition of the BCLX inhibitor A-1155463 to PARPi therapy diminishes resistance in multiple high-grade serous ovarian cancer cell lines in vitro and significantly enhances PARPi-induced tumor response in a PDX model with acquired PARPi resistance in vivo. Overall, these preclinical findings strongly support the potential of combining BH3 mimetics with PARPis to treat resistant ovarian cancer. - Source: PubMed
Publication date: 2026/09/21
Venkatachalam AnnapoornaStrathman Annabella RHou XianonCorreia CristinaMeng X WeiMcGehee Cordelia DBalczewski Emily ADuffield Laura NRossman Olivia KWong ClaraDai HaimingHurley Rachel MWagner Jill MSingh SaloniFlatten Karen SPeterson Kevin LSchneider Paula ADe Lorenzo Silvana BLarson Melissa COberg Ann LWahner Hendrickson Andrea EWu XinyanPandey AkhileshLi HuWeroha S JohnKaufmann Scott H - The advancement of nanotechnology has significantly accelerated the development of antibacterial and anticancer therapeutics for biomedical applications. Among emerging nanomaterials, layered double hydroxides (LDHs) offer several advantages, including ease of synthesis and inherent therapeutic properties. In this study, the antibacterial and anticancer activities of copper-aluminum (CuAl) LDHs were assessed. - Source: PubMed
Publication date: 2026/08/26
Shi JiayanWang YueranXu MengtingJin ShunjieYin YingKhor Kai HeZhou XuanBahadur AliShameli KamyarTeow Sin-Yeang - Cytotoxic chemotherapy is intended to eliminate transformed cells but can also provoke therapy-induced senescence, a persistent and pro-inflammatory cell state that can promote tumor progression. The molecular mechanisms that govern the apoptosis-senescence fate decision remain incompletely understood. Here, we show that the mitochondrial pore-forming proteins BAX and BAK function as a critical checkpoint that restricts entry to therapy-induced senescence. Genetic ablation of BAX and BAK markedly enhanced entry to senescence in response to multiple DNA-damaging agents, whereas loss of the BAX/BAK antagonists Bcl-xL or Mcl-1 suppressed entry to senescence and promoted cell death. Mechanistically, genotoxic stress induced BH3-only proteins, including Noxa, Bid, and Puma, creating a dependence on Bcl-xL and Mcl-1 to restrain BAX/BAK activation and maintain survival. These findings identify the Bcl-2 family network as a central regulator of entry to therapy-induced senescence, a pro-inflammatory cell state that goes beyond the mere avoidance of apoptosis. - Source: PubMed
Publication date: 2026/08/03
Gallagher Aldave AislinnVenugopalan VaishnaviGunay GokhanHamsici SerenRibeiro Ronaldo RodriguesCostigan AoifeGabrielyan AnnaEfe-Cicek HandeMartin Seamus J - Bisphenol A (BPA) is a potential risk factor for pancreatic ductal adenocarcinoma (PDAC). This study integrated network toxicology, molecular docking, molecular dynamics (MD) simulations, and TCGA clinical data analysis to explore the potential molecular mechanisms linking BPA exposure to PDAC risk. BPA-PDAC intersection targets were identified through multi-database screening, followed by protein-protein interaction (PPI) network construction to screen core hub genes. A total of 10 core hub genes were identified via PPI analysis combined with the Maximal Clique Centrality (MCC) algorithm. Molecular docking demonstrated that ESR1 exhibited one of the strongest binding affinities for BPA (-8.2 kcal/mol), and MD simulations confirmed favorable thermodynamic stability of the BPA-ESR1 complex. TCGA analysis revealed stage-dependent expression patterns: early stages showed downregulation of TP53 and BCL2, whereas advanced stages showed upregulation of BCL2L1, HSP90AA1, and HSP90AB1, while ESR1, HIF1A, and PARP1 remained consistently low. These findings suggest that BPA may promote PDAC progression by disrupting ERα-mediated endocrine signaling and impairing DNA repair through PARP1 interference, providing candidate molecular targets and a hypothesis-generating foundation for pancreatic cancer risk assessment, warranting further experimental validation. - Source: PubMed
Publication date: 2026/07/20
Li XueruWu FanZhang ZunhanAn JiayiZhou GuoqiangWang YangZhao DandanChen Xiaolu - Carbon nanotubes (CNTs) are carbon-based nanomaterials. They have been widely used in environmental technologies and in biomedical fields. - Source: PubMed
Publication date: 2026/07/01
Lotfipanah ShirinSaremi LeilaRafieitabatabaei YasaminsadatAsgari MasoudHajebrahimi Zahra