Bcl-XL, human, recombinant, full length
- Known as:
- Bcl-XL, H. sapiens, Rec., length
- Catalog number:
- G12BXL01
- Product Quantity:
- 10 ug
- Category:
- -
- Supplier:
- Giotto Biotech
- Gene target:
- Bcl- human recombinant full length
Ask about this productRelated genes to: Bcl-XL, human, recombinant, full length
- 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-XL, human, recombinant, full length
Related articles to: Bcl-XL, human, recombinant, full length
- 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 - Myeloproliferative neoplasms (MPNs) are frequently accompanied by bone marrow fibrosis and leukemic transformation, yet the cellular and molecular mechanisms that sustain apoptosis resistance and fibrotic progression remain unclear. - Source: PubMed
Publication date: 2026/06/02
Wu ChunyanWang YitingZhang QuanchaoLi ChanChen YuanzhongWu Yong - Evasion of apoptosis is a hallmark of cancer. Deregulation of BCL-XL, a member of the BCL-2 family of proteins, has been linked to the development of various tumor types. This study presents the design and synthesis of BCL-XL inhibitors with novel mono- and bicyclic cores. The new structural features were optimized to combine high binding efficiency with the opening of diverse novel vectors for additional modifications. The lead compounds exhibited picomolar affinities and significant cellular potency in the BCL-XL-dependent MOLT-4 cell line, which also translated into marked tumor growth inhibition in a xenograft study. These findings highlight the potential of BCL-XL inhibitors as therapeutic agents in cancer treatment by targeting the apoptotic intrinsic pathway. - Source: PubMed
Publication date: 2026/06/12
Timari Matyas PalPaczal AttilaHerner AndrasMolnar MarkMadarasz ZoltanNyerges MiklosBedford Simon TBrooks TeresaDavidson JamesDaniels ZoeDodsworth MarkDokurno PawelMurray James BParsons RachelSanders EmmaSmith JuliaWebb PaulWhitehead NeilHubbard Roderick EStarck Jérôme-BenoîtMaragno Ana LeticiaLe Toumelin-Braizat GaëtaneBresson LauraRocchetti FrancescaDemarles DidierColland FrédéricGeneste OlivierKotschy AndrasNovak Tibor - Current treatments of T-cell acute lymphoblastic leukemia (T-ALL) are based on intensive chemotherapy regimens which provide overall survival rates of ~85% in children and <50% in adults. Therefore, there is an unmet need for novel therapeutic options in T-ALL. Pre-clinical studies and clinical trials have demonstrated that inhibitors of BCL-XL and/or BCL-2, two anti-apoptotic proteins of the BCL-2 family, are anti-leukemic in T-ALL. However, BCL-XL inhibitors (BCL-XLi) efficacy is undermined by severe, on-target thrombocytopenia. We report here the design of a novel anti-hCD7 mAb-based ADC carrying a BCL-XL-selective inhibitor (ADC-CD7-BCL-XLi) that circumvents this significant limitation. We show that ADC-CD7-BCL-XLi efficiently kills most T-ALL cell lines. Using T-ALL PDXs we further show that (i) ADC-CD7-BCL-XLi displays potent anti-leukemic activity and is devoid of toxicity to platelets; (ii) ADC-CD7-BCL-XLi acts synergistically with venetoclax, a BCL-2 selective antagonist, to prolong leukemia remission and mouse survival; (iii) the anti-leukemic effect of the ADC-CD7-BCL-XLi+venetoclax combination can lead to cure when combined with chemotherapy. These pre-clinical data strongly support the evaluation of ADC-CD7-BCL-XLi in T-ALL patients, including as a potential bridging option to curative hematopoietic stem cell transplantation (HSCT). - Source: PubMed
Publication date: 2026/06/08
Oliveira Mariana LNuantang KanokpornHuré GrégoireÁvila-Ávila AndreaBresson LauraHaumont SandraKostova VeselaNovak TiborLe Toumelin-Braizat GaëtaneGuerlesquin JulienDemarles DidierMerdas MiraCauquil NicolasGoundiam OumouRocchetti FrancescaCourtade-Gaiani SophieValour DamienZerhouni MarwaArtus RobinDouillet-Michel EmmanuelleLaurent IsabelleDenis AliceOvreiu AlexandraDuvauchelle BorisEcsedi MatyasColland FrédéricGeneste OlivierMaragno Ana LeticiaGhysdael JacquesTran Quang Christine