Human Bcl2 Modifying Factor ELISA , BMF
- Known as:
- Human Bcl2 Modifying Factor Enzyme-linked immunosorbent assay test , BMF
- Catalog number:
- E01B0573
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Bcl2 Modifying Factor ELISA BMF
Related genes to: Human Bcl2 Modifying Factor ELISA , BMF
- 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
Related products to: Human Bcl2 Modifying Factor ELISA , BMF
Related articles to: Human Bcl2 Modifying Factor ELISA , BMF
- To overcome the critical challenges of insufficient drug targeting and restricted dendritic cell (DC) activation in chemo-immunotherapy, this study developed an innovative cross-species hybrid vesicle delivery system. By fusing extracellular vesicles derived from 4T1 tumor cells (TEV) with kiwifruit-derived extracellular vesicles (KEV), we constructed a homologous targeting hybrid vesicle carrier (TKEV). This platform was co-loaded with chemotherapeutic agent doxorubicin (DOX) and Bcl-2 siRNA (siBcl2) to form a combination therapeutic system (TKDS). Key findings demonstrate: (1) TKDS achieves precise tumor-targeted delivery, significantly enhancing tumor cell apoptosis through combined chemo-gene therapy; (2) The KEV component effectively stimulated DC maturation, enhanced antigen presentation, and increased CD8 T cell infiltration in tumors; (3) In a 4T1 murine breast cancer models, TKDS significantly enhanced antitumor efficacy through synergistic immunochemotherapy. To our knowledge, this work provides the first evidence that a cross-species vesicle fusion strategy can simultaneously enhance drug targeting and immune activation, offering a versatile and promising platform for developing highly effective and safer immunochemotherapy regimens. - Source: PubMed
Publication date: 2026/06/19
Fang ZhouWei SaichaoWang ShaoqianXu JiaqiZhang MinYin MingyuWang JunLiu Kehai - This study explored the mechanism of matrine-induced apoptosis in human retinoblastoma (RB) cell. Network pharmacology and proteomics approaches were employed to screen the intersection between the pharmacodynamic targets of matrine and the pathogenic targets of RB, and to identify the key signaling pathways underlying the anti-RB effect of matrine. Cytological experiments were used to evaluate cell proliferation, apoptosis, and the expression of PI3K/AKT pathway and apoptosis-related proteins. Results showed matrine inhibited Y79 and WERI-Rb-1 cell growth time- and dose-dependently, suppressed migration, and induced apoptosis. Integrated omics analysis identified Nuclear Receptor Subfamily 1 Group D Member 2 (NR1D2) as a primary responsive target. Matrine markedly downregulated NR1D2 expression at both the mRNA and protein levels. Matrine treatment and NR1D2 interference significantly promoted apoptosis (P < 0.05), while NR1D2 overexpression antagonized the pro-apoptotic effect of matrine. Total PI3K and AKT levels were unchanged, but their phosphorylated forms were altered; matrine-induced apoptosis correlated with Bax, Cleaved Caspase-3 upregulation and Bcl-2 downregulation. Thus, matrine inhibits RB Y79 cell growth by downregulating NR1D2, inhibiting PI3K/AKT phosphorylation and inducing RB cell apoptosis. - Source: PubMed
Publication date: 2026/06/19
Kong LiDu YangruiLan XiaomeiZheng QianHu QingqingLi TaoBin LiDu Zhiyu - B-cell lymphoma 2 (BCL-2) is an important anti-apoptotic protein in the mitochondrial cell death pathway and is biologically significant for leukemic cell survival, apoptosis resistance, drug resistance, and disease persistence. BCL-2 is clinically relevant in hematopathology and laboratory medicine, as it is a central regulator of apoptosis in several leukemia subtypes. This review evaluates BCL-2 primarily as a prognostic, treatment-stratifying, and venetoclax-related predictive biomarker in leukemia, while critically examining its more limited and context-dependent diagnostic contribution. We summarize existing data on the association of BCL-2 expression and functional dependency with leukemia biology, cytogenetic and molecular risk factors and survival. We also explore its use in distinguishing leukemic populations from non-malignant hematopoietic populations, primarily in conjunction with morphology, immunophenotyping, cytogenetics, molecular testing, and other markers of apoptosis. Laboratory considerations for clinical implementation are addressed, such as specimen selection, inter-platform variability, antibody and gating strategies, immunohistochemistry, flow cytometry, transcript-based assessment, functional apoptotic profiling, and preanalytical, analytical, and interpretative variability. We also discuss the clinical relevance of BCL-2 in venetoclax-based therapy, where dependence on BCL-2 may be more informative than expression. Overall, BCL-2 is better supported as prognostic and treatment-stratifying marker than a diagnostic marker in leukemia. To move BCL-2 assessment into routine laboratory practice, it will be necessary to establish harmonized thresholds for BCL-2 assays and to validate the analytical workflow and result in prospective studies. This review outlines the potential and current challenges of BCL-2 as an emerging biomarker in human leukemia within a laboratory medicine framework. - Source: PubMed
Publication date: 2026/06/19
Rehman Zia UrKhan AbidaImran MohdSingla NeelamKamal Mohammad AzharKhalid MohammadAli Md ImtiazBakht Md Afroz - A series of new compounds was designed and synthesized based on the pronounced anticancer activities of the thiazole ring and hydrazone groups against breast cancer cells. IR, H NMR, C NMR (decoupled and APT), F NMR, 2D NMR (HSQC), HRMS and elemental analysis data were used to confirm the structures of the compounds. Cytotoxicity was assessed by the MTT assay, while immunoperoxidase staining was used to examine the distribution of caspase-3, BAX, Bcl2, cytochrome c, Ki-67, RIPK1, RIPK3, and MLKL in breast cancer cell lines (M4A4 and MCF-7). Compounds 4b, 4c, 4d, 4g, 4h, and 4l were the most effective derivatives in the series against MCF-7 and M4A4 cancer cells, with IC values of 51-106 μM and 12.87-100 μM, respectively. Molecular docking and molecular dynamics (MD) simulations were performed to elucidate the interactions between compound 4l, which has the best BAX: Bcl2 ratio, and the BAX and Bcl2 proteins. In addition, molecular docking and MD simulations showed that compound 4l stably binds within the Bcl2 BH3-binding groove, maintaining key interactions with ASP108, TYR105, and ARG143 during the 300 ns simulation. The RMSD remained below 2.5 Å after equilibration, supporting the structural stability of the complex. - Source: PubMed
Publication date: 2026/06/15
Tok FatihEnsarioğlu Hilal KabadayıBaşoğlu FaikaBecer EdaKıyak NadireVatansever Hafize Seda - Morin (2',3,4',5,7-pentahydroxyflavone) is a polyphenolic dietary flavonoid found naturally in foods and has demonstrated anticancer effects in multiple preclinical models. This narrative review presents a comprehensive pharmacological analysis of morin's capacity to modulate apoptosis and autophagy, which are convergent pathways of programmed cell death (PCD) in both solid and hematological malignancies. Morin has been reported to influence intracellular reactive oxygen species (ROS) levels and disrupt the mitochondrial membrane potential (ΔΨm), thereby affecting the AMPK-mTOR-ULK1-Beclin-1 autophagic pathway. This review synthesizes preclinical data obtained from in vitro cancer cell line models, in vivo xenograft and chemical-induced tumor systems, and hypothesis-generating in silico molecular docking and network pharmacology studies. The significant crosstalk between apoptosis and autophagy appears to involve the Bcl-2/Beclin-1 pathway, cleavage of autophagy-related proteins by caspases, and shared redox stress. Mechanistic interpretation should be used with caution, as several studies have used associative molecular end points, and the accumulation of LC3-II does not equate to complete autophagic flux. Novel nanoformulation-based drug delivery strategies, the potential of chemo-sensitization in drug-resistant tumor models, and available preclinical safety and toxicology data are examined in the context of the pharmacokinetic limitations of morin, such as poor oral bioavailability, low aqueous solubility, intestinal metabolism, P-glycoprotein efflux, and limited clinical pharmacokinetic validation. Pharmacological studies suggest that morin may be classified as a multi-target phytopharmacological agent. However, more rigorous studies are required for target validation, including autophagy flux assays, clinically relevant tumor models, and pharmacokinetic optimization, before it can be translated into a therapeutic application. - Source: PubMed
Publication date: 2026/06/19
Alharbi Khalid Saad