Polyclonal Bcl-2 (NT)
- Known as:
- Polyclonal Bcl-2 (NT)
- Catalog number:
- pc-472
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Polyclonal Bcl-2 ()
Related genes to: Polyclonal Bcl-2 (NT)
- 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: Polyclonal Bcl-2 (NT)
Related articles to: Polyclonal Bcl-2 (NT)
- - Source: PubMed
Publication date: 2025/09/01
Zohreh Jadali - Acute Myeloid Leukemia (AML) is characterized by the clonal expansion of undifferentiated myeloid precursors and is associated with notably higher incidence and mortality rates in the elderly population. While the BCL-2 inhibitor Venetoclax has transformed the therapeutic landscape for patients with AML who were ineligible for intensive therapy, primary and acquired resistance remained major obstacles to durable responses. - Source: PubMed
Publication date: 2026/05/25
Yang FanWu HangYao JingPeng XueluYang AiyunWen TaoMeng JieLiu JianZhang YuWang TaoXu Haiyan - Diphtheria toxin (DT) has been reported to exhibit cytotoxic effects in several cancer models; however, the molecular mechanisms underlying its apoptotic activity remain incompletely understood. In our previous study, DT was shown to induce cytotoxic and apoptotic responses in HT-29 colorectal cancer cells, characterized by the upregulation of pro-apoptotic genes and suppression of anti-apoptotic signaling. Building on these findings, the present study aimed to explore the potential molecular context underlying DT-induced transcriptional alterations using computational and bioinformatic approaches. Molecular protein-protein docking was performed to evaluate the possible interaction between DT and the anti-apoptotic protein Bcl-2. In parallel, previously obtained qRT-PCR gene expression data from HT-29 cells were reanalyzed to assess coordinated transcriptional responses associated with DT exposure. Network analysis using the STRING database indicated that DT-responsive genes form a functionally connected interaction network associated with apoptosis, cellular stress responses, and cell-cycle regulation. Principal component analysis and hierarchical clustering confirmed consistent differences in gene expression patterns between treated and control samples. Docking results suggested a potential interaction between DT and the BH3-binding groove of Bcl-2, supported by hydrogen bonding and hydrophobic contacts. Pathway enrichment analyses further linked the analyzed genes to apoptosis-related pathways, including FoxO and p53 signaling. Collectively, these findings provide an integrated framework suggesting that DT-induced cytotoxicity in HT-29 cells may involve coordinated transcriptional responses and potential structural interaction with Bcl-2, highlighting regulatory networks associated with apoptosis, cellular stress, and cell-cycle control. - Source: PubMed
Ercan ElifYalcinkaya TugbaLevent BelkisCarhan Ahmet - Senescent cells, which have irreversibly arrested cell proliferation and a senescence-associated secretory phenotype, are characterized by the production of proinflammatory cytokines and growth factors. The selective clearance of senescent cells might have beneficial effects on physiological functions or aging-related diseases. Senolytic drugs, such as ABT-263, an inhibitor of BCL-2 family proteins, selectively kill senescent cells. In the present study, we investigated the effect of IL-4 and IL-13, which contribute to type 2 immunity and fibrosis, on ABT-263-induced apoptosis in senescent cells. Doxorubicin was used to induce senescence in TIG-1 cells, a normal diploid fibroblast line commonly used to study cellular senescence. Although ABT-263 selectively induced apoptosis in senescent TIG-1 cells at lower concentrations than were required to induce apoptosis in non-senescent cells, IL-4 and IL-13 suppressed ABT-263-induced apoptosis in senescent TIG-1 cells. Pharmacological experiments using inhibitors revealed that the suppressive effects of IL-4 and IL-13 involved the IL-4Rα/JAK/STAT6 signaling pathway. We found that IL-4 and IL-13 altered the expressions of molecules involved in extracellular matrix and cell adhesion, and induced phosphorylation of the downstream FAK/Akt/GSK3β signaling pathway. In addition, senescent TIG-1 cells treated with IL-4 and IL-13 showed increased glucose consumption, and the suppressive effect of IL-4 and IL-13 was partially abolished by inhibitors of the glucose metabolic pathway. Taken together, IL-4/IL-13 signaling had a suppressive effect on ABT-263-induced apoptosis in senescent human fibroblasts. These results suggest that a combination of senolytic drugs and inhibitors targeting IL-4/IL-13 signaling might be effective for aging-related diseases. - Source: PubMed
Publication date: 2026/06/01
Nishinaka TakashiWake HidenoriWatanabe MasahiroToyomura TakaoMori ShujiNishibori MasahiroTakahashi Hideo - Myeloid cell leukemia 1 (Mcl-1) is a pivotal anti-apoptotic protein, whose overexpression drives tumorigenesis, progression and drug resistance in multiple hematological malignancies. Herein, guided by a bioisosteric design, we replaced the sulfonyl group with a drug-like sulfonimide linker and synthesized a novel series of Mcl-1 inhibitors based on our previous lead compound DDO-8201. Among them, compound 52 displayed potent and selective Mcl-1 inhibition (K = 0.024 μM) with at least 400-fold selectivity over other Bcl-2 family proteins. It showed an IC of 0.45 μM against Mcl-1-sensitive Molm-13 cells, superior to A1210477, and retained good activity against Venetoclax-resistant Molm-13 cells (Molm-13_VenR, IC = 1.16 μM). Moreover, 52 exhibited favorable drug-like properties, including good membrane permeability (Pe = 11.11 × 10 cm/s), water solubility (78.5 μg/mL), high stability (HLM, t = 1.83 h) and oral bioavailability (F% = 32%). This study provided a new strategy for Mcl-1 inhibitor development, and 52 represents a promising candidate for overcoming Venetoclax resistance. - Source: PubMed
Publication date: 2026/05/29
Wang JunjieXu KeZhu PengjuZhao ZiquanWen ShuaiZhao JinglongXin YabinYou QidongJiang ZhengyuLu Mengchen