Bcl-2 Oncoprotein;
- Known as:
- Bcl-2 Oncoprotein;
- Catalog number:
- Mob 130-05
- Product Quantity:
- 0.5ml
- Category:
- -
- Supplier:
- Diagnostic Biosystems
- Gene target:
- Bcl-2 Oncoprotein;
Related genes to: Bcl-2 Oncoprotein;
- 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: Bcl-2 Oncoprotein;
Related articles to: Bcl-2 Oncoprotein;
- Acute myeloid leukemia (AML) remains a highly lethal hematologic malignancy characterized by metabolic reprogramming, therapeutic resistance, and poor survival, particularly in older patients. Nicotinamide adenine dinucleotide (NAD⁺) metabolism has emerged as a central driver of AML progression, and recent studies have identified solute carrier family 25 member 51 (SLC25A51) as the primary mitochondrial NAD⁺ transporter in mammalian cells. SLC25A51 regulates mitochondrial redox balance, oxidative phosphorylation, and tricarboxylic acid (TCA) cycle activity, thereby sustaining leukemic proliferation and survival. Structural studies have elucidated its six-transmembrane helix architecture, salt-bridge-mediated transport mechanism, and stabilization by cardiolipin binding. Functional investigations demonstrate that SLC25A51 overexpression correlates with poor prognosis, while its depletion disrupts mitochondrial metabolism, induces apoptosis, and suppresses AML progression in vivo. Therapeutically, pharmacologic inhibition of SLC25A51 with fludarabine, or its combination with hypomethylating agents, such as 5-azacytidine, enhances antileukemic efficacy by perturbing metabolic and epigenetic regulation. Moreover, SLC25A51 expression may serve as a predictive biomarker for mitochondrial-targeted therapies, such as complex I inhibitors. Future translational research should focus on developing selective inhibitors, optimizing combination strategies with demethylating agents and BCL-2 inhibitors, and validating its prognostic significance in clinical cohorts. Collectively, SLC25A51 represents a promising metabolic target with potential to overcome therapeutic resistance and improve patient outcomes in AML. Furthermore, this review discusses its potential implications across distinct genetic subtypes of AML (e.g., mutations in TP53, NPM1, and RAS), thereby highlighting key directions for future translational research. - Source: PubMed
Publication date: 2026/07/19
Rong ChunmengChen RuixiuLou HanqiXia YongmingDuan Shiwei - Pyrogallol, a polyphenolic compound, exhibits diverse activities, including antibacterial, antifungal, and antiviral effects; however, its anticancer potential has only been examined in a very few cancers and remains unexplored in T cell lymphoma. Hence, the present study is designed to elucidate the antitumor potential of pyrogallol against T cell lymphoma along with possible implication of modulated glucose metabolism and immune evasion. The experimental findings of this investigation show tumor-specific cytotoxicity of pyrogallol against T lymphoma cells. Further, pyrogallol has been shown to mediate G2/M cell cycle arrest by downregulating cyclin B1 and c-Myc expression, and induce apoptosis by altering ROS levels, mitochondrial membrane potential, and the expression of apoptosis regulators, namely Bcl2 and cleaved caspase 3, in T lymphoma cells. Furthermore, pyrogallol is observed to shift glucose metabolism towards oxidative phosphorylation by suppressing GLUT1, GLUT3, HKII, PKM2, PDK1, PDK3, and HIF-1α levels. Moreover, it suppresses the immune evasion ability of T lymphoma cells through deregulating 'do not eat me' and 'find me' signals, specifically PD-L1, CD-24 and CD-47, and S1P and LPC, respectively. Notably, the disrupted AKT pathway was found to play a critical role in pyrogallol-mediated T cell lymphoma growth inhibition. Overall, our investigation demonstrates that pyrogallol exerts tumor growth inhibitory effect in T lymphoma cells by modulating the cell cycle, apoptosis, glucose metabolism, and immune evasion in an AKT-dependent manner. - Source: PubMed
Publication date: 2026/07/17
Kumar AbhishekKumar MukeshRai SiddharthSonker PratishthaKumar Ajay - Bronchopulmonary dysplasia (BPD) is a prevalent chronic lung disease among preterm infants, largely attributed to hyperoxia-induced injury to alveolar epithelial cells. Excessive endoplasmic reticulum (ER) stress plays a vital role in BPD progression. SRPRA, a subunit of the ER-localized SRP receptor, is upregulated in BPD, while its function and link with ER stress remain largely unclear. This study aimed to explore the role of SRPRA in hyperoxia-induced BPD and its underlying mechanism. - Source: PubMed
Publication date: 2026/07/19
Tan YanlinXiong ShisiNi WenchangWang LiyanBian Junmei - This study aimed to investigate the mechanisms through which Erzhi Tiangui Formula (EZTG) mitigates age-related ovarian aging in mice through the Nrf2/HO-1 antioxidant pathway. - Source: PubMed
Publication date: 2026/07/18
Li XiufangWang ZhongqingZhang XiuqingWang HuidanHan XuZheng YeSun MeiWu HaicuiLian Fang - The introduction of venetoclax (a BCL2 inhibitor) and targeted therapies, including inhibitors of CD33, FLT3, IDH1, IDH2, and menin, has expanded treatment options for newly diagnosed acute myeloid leukemia (AML). In younger, fit patients, the primary goal remains long-term survival, which in most cases is secured through allogeneic stem cell transplant. Transplant in first complete remission is recommended for FLT-ITD, TP53 mutated, KMT2A rearranged, AML with other adverse genetic abnormalities, and is considered in most intermediate-risk patients. It is also recommended in relapsed/refractory disease or persistent measurable residual disease (MRD). The role of intensive chemotherapy, such as cytarabine (7) plus anthracycline (3), is limited to patients with core-binding factor AML, NPM1 mutation, CEBPA bZIP mutation and those with intermediate-risk disease. Intensive regimens such as FLAG-IDA and CLIA plus venetoclax have shown impressive long-term outcomes, but their use is not widespread. In FLT3 mutated AML, 7 + 3 plus an FLT3 inhibitor (midostaurin or quizartinib) remains a standard, with venetoclax-hypomethylating agent-FLT3 inhibitor triplets emerging as an alternative. Similarly, in IDH1/2 mutated AML, venetoclax-hypomethylating agent with or without IDH1/2 inhibitor combinations challenge intensive chemotherapy approaches. Patients with TP53 mutations or other adverse-risk features, where intensive chemotherapy is known to be less effective, should be referred for clinical trials. There remains ongoing debate regarding optimal management of fit patients with newly diagnosed AML without targetable mutations, as emerging data suggest that venetoclax- hypomethylating agents may be comparable to intensive chemotherapy in selected patients proceeding to transplant. Accordingly, treatment decisions should be individualized to maximize remission while minimizing toxicity. - Source: PubMed
Publication date: 2026/07/18
Gangat NaseemaRavandi Farhad