ELISA Human , Bcl-2
- Known as:
- Enzyme-linked immunosorbent assay test Human , Bcl-2
- Catalog number:
- RBMS244/3R
- Product Quantity:
- 96 wells (1 kit)
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- ELISA Human Bcl-2
Related genes to: ELISA Human , Bcl-2
- 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: ELISA Human , Bcl-2
Related articles to: ELISA Human , Bcl-2
- Myelodysplastic syndromes (MDS) are clonal hematopoietic malignancies that pose a serious health threat. Current therapies include symptomatic treatments for low-risk and hypomethylating agents for high-risk MDS. However, many patients develop resistance to hypomethylating drugs. (Exportin 1) XPO1 inhibition has shown efficacy in inducing tumor cell death by blocking the nuclear export of oncogenes; nevertheless, the role of XPO1 inhibition in MDS remains unexplored. - Source: PubMed
Publication date: 2026/04/20
Liu XiaohanHuang LeiWang JunzhuGuo YixuanShen HongliZhao XianghongYue LanzhuLiu ZhaoyunFu Rong - Chikungunya virus (CHIKV) infection can induce acute kidney injury (AKI) and may be fatal in severe cases, yet effective therapeutic strategies remain unclear. This study integrated computational analysis (network pharmacology and molecular docking) with experiments to evaluate the protective potential of oxymatrine against CHIKV-induced AKI and to explore its underlying mechanisms. Network pharmacology analysis identified 605 overlapping targets between CHIKV- and AKI-related genes, with core targets including TNF, AKT1, IL6, IL1B, and TP53, which were primarily enriched in the PI3K/AKT signaling pathway. RT-qPCR analysis and molecular docking further indicated that oxymatrine may interact with 18 targets, such as BAX, BCL2, and TLR4, thereby modulating CHIKV-associated PI3K/AKT signaling. experiments showed that oxymatrine at concentrations of 250-2,000 μM significantly increased the viability of HEK293T cells infected with CHIKV at a MOI of 0.01 for 24 h, with an average increase of approximately 25.8%. At these concentrations, oxymatrine reduced the expression of the CHIKV entry factor and regulated the PI3K/AKT, NF-κB, and TNF signaling pathways, which may contribute to the inhibition of viral replication. Further analysis revealed that CHIKV-induced AKI involved 75 ferroptosis-related targets and was closely associated with inflammatory responses. Oxymatrine may attenuate these effects through the regulation of targets such as SIRT3, AR, and FURIN. Consistently, ELISA results demonstrated that 1,000 μM oxymatrine significantly decreased the levels of IL-1β, TNF-α, and IL-6 in HEK293T cells infected with CHIKV. In conclusion, these findings suggest that oxymatrine may protect against CHIKV-induced AKI by limiting viral replication, modulating PI3K/AKT and NF-κB/TNF signaling pathways, suppressing inflammation, and regulating ferroptosis-related processes. - Source: PubMed
Publication date: 2026/04/02
Xin JiaLiangLi FangJunKang LuLuYang JieWang HaiTongWang WeiFeng ShengLiao XinFeiLi WenJieZhang He - Pancreatic cancer has a poor prognosis and is highly aggressive and deadly. Most pancreatic cancer diagnoses are adenocarcinomas, which account for more than 90 % of all cases. Developing effective therapeutic strategies requires an understanding of the molecular mechanisms associated with pancreatic cancer progression. Small nucleolar RNA 64 (SNORA64) was presented as a predictive marker for pancreatic cancer stages in our previous study. SNORA64 showed a gradual loss of its expression throughout the carcinogenesis process, and it inhibited metastasis by interfering with epithelial to mesenchymal transition (EMT). In this study, we investigated the role of SNORA64 on an intrinsic apoptotic pathway in pancreatic cancers by using human pancreatic cell line derived from adenocarcinoma PK-8 with SNORA64 knockdown and the scramble to compare with. - Source: PubMed
Publication date: 2026/01/16
Alfardan Rana - Recent studies have highlighted the critical role of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3) in inflammation, with inhibitors like 3PO showing therapeutic potential in various inflammatory diseases. However, its effect on asthma inflammation remains unclear. - Source: PubMed
Publication date: 2026/04/02
Huang SiqingWei ShunaLuo FangCheng Yuanxiong - Diabetes mellitus is a chronic metabolic disorder in which endothelial dysfunction plays a pivotal role in disease progression. (PSP) exhibit multiple biological activities, including antioxidant effects, anti-apoptotic action, and regulation of lipid metabolism. However, the mechanisms by which PSP protects against diabetic endothelial injury remain poorly understood. Therefore, this study aimed to elucidate the protective role and underlying mechanisms of PSP in diabetes-induced vascular endothelial injury. In this study, PSP treatment markedly alleviated diabetes-induced vascular endothelial injury, reduced serum TG and LDL levels in streptozotocin (STZ)-induced diabetic rats. Proteomic enrichment analysis revealed that PSP modulates multiple molecular pathways related to oxidative stress, lipid metabolism, and apoptosis. Further experiments showed that PSP treatment restored mitochondrial membrane potential, enhanced cell viability, suppressed Caspase-3 and Bax expression, and upregulated Bcl-2 to attenuate palmitic acid (PA)-induced apoptosis in endothelial cells. Moreover, PSP reduced lipid peroxidation products (ROS and MDA) and upregulated the expression of Nrf2 and GPX4. In conclusion, PSP effectively alleviates diabetes-induced vascular endothelial injury by improving lipid metabolism, inhibiting apoptosis and oxidative stress, partly through activation of the Nrf2/GPX4 pathway. These findings highlight the potential of PSP as a therapeutic agent for diabetes. - Source: PubMed
Publication date: 2026/04/07
Wu DongdongZhao JingYang QifanFang RourouXu Shouzhu