BCL2L10 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- BCL2L10 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb101255
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- BCL2L10 antibody Polyclonal Antibodies Primary antibodies
Related genes to: BCL2L10 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- BCL2L10 NIH gene
- Name:
- BCL2 like 10
- Previous symbol:
- -
- Synonyms:
- Diva, Boo, BCL-B
- Chromosome:
- 15q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-21
- Date modifiied:
- 2016-10-05
Related products to: BCL2L10 antibody Polyclonal Antibodies Primary antibodies
Related articles to: BCL2L10 antibody Polyclonal Antibodies Primary antibodies
- Diffuse large B-cell lymphoma (DLBCL) is characterized by marked heterogeneity between GCB and non-GCB subtypes. Here, we identified BCL2L10 as a non-GCB-specific oncogene through integrated bioinformatics, clinical validation, and functional assays. BCL2L10 was significantly upregulated in non-GCB DLBCL at both mRNA and protein levels. High BCL2L10 expression served as an independent adverse prognostic factor and correlated with advanced clinical stage. Gene set enrichment analysis linked BCL2L10 to biosynthetic and stress-response pathways. Functional assays demonstrated that BCL2L10 knockdown selectively suppressed proliferation in non-GCB DLBCL cells, whereas overexpression only mildly promoted GCB cell growth. Our findings identify BCL2L10 as a novel subtype-specific prognostic biomarker and therapeutic target for high-risk non-GCB DLBCL. - Source: PubMed
Publication date: 2026/05/20
Yu LiliWu ShiwenLi LiangliangYang JincaiMan JianchengSong FeixueZhao Li - Esophageal cancer remains a significant global health challenge with increasing rates of incidence and mortality, particularly esophageal squamous cell carcinoma (ESCC), with higher prevalence in Asia. This study aims to investigate the cytotoxicity and potential cell death mechanisms (i.e., apoptosis, necroptosis, ferroptosis, and pyroptosis) induced by three newly synthesized benzamidine derivatives (NBDs) against the ESCC KYSE-150 cell line. MTT cell viability assay was used to assess the cytotoxic effect of the NBDs on the ESCC cell line, KYSE-150, and the normal esophageal epithelial cell line, HET-1A. In silico molecular simulation and binding free energy calculation methods were used to validate the potential cell death targets (s) involved in ESCC cells upon interaction with the NBDs. The results showed that the cytotoxic effect of all three NBDs on KYSE-150 outperformed 5-fluorouracil (5-FU), with NBD 3 producing the highest cytotoxicity (IC50: 21.57 µM), followed by NBD 2 (IC50: 34.17 µM) and NBD 1 (IC50: 37.75 µM). Among the three NBDs, NBD 3 was the most potent in inducing cytotoxicity in KYSE-150 cells. In silico molecular docking revealed that NBD 2 and NBD 3 exhibited relatively strong binding affinities (< -7.0 kcal/mol) toward multiple protein targets, including Caspase-9, BIM BH3 peptide, BCL2 Antagonist/Killer (BAK), Tumor Necrosis Factor Receptor (TNFR), Fas Cell Surface Death Receptor (FAS), BCL2-Like 1, long isoform (BCL-XL), BCL2-Like 2 (BCL-W), BCL2-Like 10 (BCL2L10), Heat Shock Protein 70 (Hsp70), Heat Shock Protein 90 (Hsp90), Receptor-Interacting Serine/Threonine-Protein Kinase 1 (RIPK1), Dynamin-1-Like Protein (DNM1L), Apoptosis-Inducing Factor, Mitochondria-Associated 2 (AIFM2), and Absent in Melanoma 2 (AIM2), molecular simulation results further confirmed the stability, structural compactness and residual flexibility. In addition, the binding free-energy calculations characterized the relative binding strengths of these derivatives toward the selected pathway targets. These computational results, together with the docking-derived interaction profiles, support the prediction that these programmed cell-death pathways may be potentially engaged in ESCC upon interaction with the NBDs. While the analyses are consistent with possible involvement of these mechanisms, they do not constitute experimental validation and should be interpreted as computational indications rather than confirmatory evidence. This study provides insights into the potential anticancer activities and the mechanistic pathway of NBDs in ESCC. - Source: PubMed
Publication date: 2026/04/13
Loh Trisha Krishni Foong YunLee Michelle FeliciaAgouni AbdelaliFuloria Neeraj KumarFuloria ShivkanyaSekar MahendranSaleem ShoaibGopinath Subash C BKhan AbbasWu Yuan Seng - This study aims to explore the potential molecular mechanisms by which di (2-ethylhexyl) phthalate (DEHP) exposure induces pulmonary arterial hypertension (PAH). - Source: PubMed
Publication date: 2026/03/20
Li HuaJiang YingchunLi Jijia - Curcumin, a major phytochemical derived from Curcuma longa, has been shown to enhance the efficacy of chemotherapeutic agents such as doxorubicin, 5-fluorouracil, and cisplatin by overcoming drug resistance, making it a promising adjunct in the treatment of glioblastoma. However, the global gene-expression changes triggered by curcumin in glioblastoma remain underexplored. In this study, we investigated the effects of curcumin on human glioblastoma (U87 MG) cells, where it significantly reduced cell viability and proliferation in a dose- and time-dependent manner and induced apoptosis without affecting senescence. Transcriptomic analysis revealed 5036 differentially expressed genes, with pathway enrichment identifying 13 dysregulated cancer-associated pathways. Notably, curcumin modulated several key regulators involved in MAPK, Ras, TGF-β, Wnt, Cytokine, and TNF signaling pathways. Several apoptosis and cell cycle-associated genes, including PRKCG, GDF7, GDF9, GDF15, GDF5, FZD1, FZD2, FZD8, AIFM3, TP53AIP1, CRD14, NIBAN3, BOK, BCL2L10, BCL2L14, BNIPL, FASLG, GZMM, TNFSF10, TNFSF11, and TNFSF4, were significantly altered. Several pro-apoptotic and anti-BCL, cell-cycle-regulated genes were modulated following curcumin treatment, emphasizing its potential role in curcumin-mediated anti-tumor effects. This study provides insight into the molecular mechanisms underlying curcumin's action against glioblastoma. - Source: PubMed
Publication date: 2025/05/09
Mashozhera Nicole TendayiReddy Chinreddy SubramanyamRanasinghe Yevin NenukaNatarajan PurushothamanReddy Umesh KHankins Gerald - Phthalates are synthetic chemical compounds commonly used in consumer products. Neonates are often exposed to phthalate mixtures, but the effects of neonatal exposure to phthalate mixtures on ovarian health are unclear. Thus, this study tested the hypothesis that neonatal exposure to an environmentally relevant phthalate mixture alters neonatal ovarian function by disrupting steroidogenesis and cell cycle regulation and promoting inflammation, oxidative stress, and apoptosis. CD-1 neonatal mice were orally dosed with corn oil or a phthalate mixture (10, 20, 100 μg/kg/day) daily from post-natal day (PND) 3 to PND 8. Sera and ovaries were collected on PND 8 and PND 10 to quantify follicle numbers and to measure phthalate metabolites, protein levels, and expression of key markers involved in ovarian health. At PND 8, neonatal exposure to the mixture increased the levels of the phthalate metabolites (mono-ethyl phthalate and mono(2-ethylhexyl) phthalate) and C-reactive protein in the sera and it decreased the number of primordial follicles and ovarian expression of Il1-r2. Additionally, the mixture increased the expression of steroidogenic regulators (Cyp17a1 and Lhcgr) and a pro-apoptotic factor (Bad) in comparison to controls. At PND 10, the mixture decreased the number of primordial follicles and the expression of Cyp17a1, Bad, Bax, Fas, and Cdkn1a, and increased expression of Lhcgr, Fshr, and Bcl2l10 in comparison to controls. Collectively, these data indicate that neonatal exposure to an environmentally relevant phthalate mixture decreases the health of the neonatal ovary. - Source: PubMed
Publication date: 2025/05/04
Fletcher Endia JStubblefield Winter SSeaton Taylor ASantacruz-Márquez RamsésLaws Mary JGonyea Teegan MDean Angela ELi ZhongFlaws Jodi A