Bcl2 ELISA kit
- Known as:
- Bcl2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-Bcl2-Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- Bcl2 ELISA kit
Related genes to: Bcl2 ELISA kit
- 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
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- Therapeutic advances in chronic lymphocytic leukaemia (CLL) have made treatment selection far more nuanced than in the chemoimmunotherapy era. Patients now have access to two principal therapeutic strategies: continuous therapy with Bruton's tyrosine kinase inhibitors (BTKi) or fixed-duration regimens combining venetoclax with CD20 monoclonal antibodies and/or BTKis. These strategies carry fundamentally different safety profiles, monitoring requirements, and logistical demands, necessitating a treatment-specific approach to fitness assessment. - Source: PubMed
Publication date: 2026/08/27
Al-Asa Apos D YousefAlshemmari Salem HQasem Nabeel MohammadAl Battah AfafYassin Mohamed A - Drug-induced nephrotoxicity is an alarming trigger for kidney injury. It is linked to a high rate of illness and fatality, with limited treatment options. Herein, we aimed to unravel the phytochemical profile and understand the protective activity of the aqueous methanolic extract (AME) of P.cattleianum Sabine (Myrtaceae) aerial parts against nephrotoxicity induced by gentamicin (GNT) in rats for the first time. The extract was chromatographed and analyzed using an LC-ESI-TOF-MS system. For the in vivo model, rats received the AME at doses of 200, 400, and 800 mg/kg/day orally for 14 days. The phytochemical results revealed the tentative identification of ninety metabolites, including twelve phenolic acids, fifty-one flavonoids, one proanthocyanidine, one lignan, four coumarins, three terpenes, four organic acids, two stilbenes, seven sugar derivatives, and five miscellaneous compounds. At 800 mg/kg, the AME significantly reduced the KW/BW ratio by 14.7%, BUN by 45.2%, creatinine by 57.6%, and Kim-1 by 57.3%. Oxidative stress markers MDA and 8-OHdG were lowered by 47.5% and 67.4%, respectively, while antioxidant markers GSH and SOD increased by 2.7- and 2.6-fold. The AME also restored HO-1 (4.6-fold increase) and Nrf2 (92.2-fold increase, relative to the GNT-treated group), and suppressed TNF-α, IL-1β, and NF-κB by 53.3%, 64.7%, and 58.9%, respectively. Apoptosis was reduced (Bax ↓64%, cytochrome c ↓58.8%, Bcl-2 ↑threefold), with marked histological improvements confirming nephroprotection. In all, the AME is promoted as an alternative remedy for controlling nephrotoxicity triggered by GNT. However, quantifying and isolating the major constituents and validating the clinical safety are among our future directions. - Source: PubMed
Publication date: 2026/08/27
Hassan Hoda MKhazaal Heba TMoharram Fatma AEl-Sayed Elsayed KMusa Abdalrhman EAhmed Asmaa AElsayed Heba EMohammed Nermine M - Epitranscriptomics has rapidly evolved into a central layer of post-transcriptional gene regulation in cancer, yet its mechanistic contribution to regulated cell death remains incompletely resolved. This review critically examines how RNA modifications principally N⁶-methyladenosine (m⁶A), alongside 5-methylcytosine (mC), N⁷-methylguanosine (m⁷G), pseudouridylation (Ψ), and adenosine-to-inosine (A-to-I) editing reprogram apoptotic and ferroptotic thresholds in malignant cells. It highlights that m⁶A does not exert uniform effects; rather, outcomes are dictated by site specificity, reader stoichiometry, and cellular context, with opposing roles observed in the regulation of BCL-2 family signaling and the SLC7A11-GPX4 antioxidant axis. The analysis extends beyond m⁶A to evaluate emerging, yet often under-validated, evidence implicating mC in ferroptosis resistance, A-to-I editing in immune evasion, and m⁷G/Ψ in translational control of survival programs. Importantly, the review integrates tumor microenvironmental pressures including hypoxia, reactive oxygen species, and immune signaling-as dynamic modulators of epitranscriptomic machinery, thereby linking RNA chemistry to adaptive stress responses and therapeutic resistance. Despite rapid technological advances, including MeRIP-seq, crosslinking-based mapping, and nanopore direct RNA sequencing, the field remains constrained by limited resolution, lack of quantitative stoichiometry, and insufficient site-specific functional validation. Many conclusions are derived from global perturbation of epitranscriptomic enzymes, obscuring causal attribution to individual modified transcripts. From a translational perspective, targeting writers, erasers, and readers offers promise for sensitizing tumors to cell death; however, pleiotropy, context dependency, and potential toxicity present significant barriers. Overall, this review argues that while epitranscriptomics represents a compelling regulatory axis in cancer cell death, advancing the field will require integrative, high-resolution, and functionally precise approaches to move beyond correlative frameworks toward mechanistic and clinically actionable insights. - Source: PubMed
Publication date: 2026/08/27
Mukherjee Anirban GoutamBharti Ankit KumarMathew Deepthi MariaVarma Bhavani ManojPradhan SristyGopalakrishnan Abilash Valsala - Aflatoxin B1 (AFB1) is one of the most potent naturally occurring mycotoxins and has been implicated in reproductive toxicity. The present study is aimed at evaluating the time-dependent effects of experimental AFB1 exposure on ovarian follicular dynamics, reproductive hormone profiles, and intrinsic apoptosis-related markers in female rats. - Source: PubMed
Poursadeghi FarbodRazi MazdakAmniattalab Amir - Apoptosis is a core program regulating organismal homeostasis and plays a pivotal role in the onset and progression of most diseases. Increasing evidence in recent years indicates that mitochondria are not only central to cellular metabolism but also play a pivotal role in regulating apoptosis. However, no systematic review elucidating how mitochondria finely regulate apoptotic processes through multidimensional mechanisms, including apoptosis-resistant diseases such as cancer. This paper systematically summarizes the molecular mechanisms by which mitochondria mediate apoptosis. We focus on the regulation of cytochrome (Cyt c) release by the Bcl-2 protein family and the activation of downstream caspase cascades. Furthermore, we provide an in-depth analysis of intrinsic factors, including mitochondrial structural remodeling (membrane rupture, cristae remodeling, and membrane lipid redistribution), dynamics imbalance (fusion, fission, and mitophagy), and mitochondrial DNA abnormalities, as well as extrinsic factors involving interorganelle interactions with the endoplasmic reticulum, lysosomes, and other organelles. Additionally, we review clinical and preclinical advances in drugs targeting these pathways. This review aims to provide a comprehensive perspective on the complex network of mitochondrial regulation of apoptosis and offer valuable insights for developing novel clinical therapeutic strategies for cancer and other diseases. - Source: PubMed
Publication date: 2026/08/26
Tan RubinZhao JinmingWang RongShi YueChen ZaozaoMa YixuanLi NaDuan WenqingLin DuoZhang Chunxiang