Human Bcl2 Associated Death Promoter ELISA , BAD
- Known as:
- Human Bcl2 Associated Death Promoter Enzyme-linked immunosorbent assay test , BAD
- Catalog number:
- E01B0633
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Bcl2 Associated Death Promoter ELISA BAD
Related genes to: Human Bcl2 Associated Death Promoter ELISA , BAD
- 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 Associated Death Promoter ELISA , BAD
Related articles to: Human Bcl2 Associated Death Promoter ELISA , BAD
- Lung cancer is one of the malignant tumors with the highest mortality in the world. Quercetin (Qu) is a flavonoid compound isolated from Tetrastigma hemsleyanum Diels & Gilg (SYQ), which has multi-target anti-tumor activity. However, there are problems such as low extraction purity, poor water solubility, and difficulty in targeted delivery. Its anti-lung cancer mechanism remains to be elucidated. - Source: PubMed
Publication date: 2026/06/06
Wang DayangYe JiashuoWang ZiyanZou JiaxinYu BingCong Hailin - Polystyrene nanoplastics (PS-NPs) are an emerging class of environmental contaminants with increasing concern regarding their potential effects on reproductive development. This study examined whether maternal lactational exposure to PS-NPs is associated with alterations in ovarian growth, structure, and function in female rat offspring. The dams were administered PS-NPs at doses of 0, 0.1, 1, or 10 mg/kg/day exclusively during the 21-day lactation period. Female offspring were evaluated on postnatal days 30 (PD30) and 60 (PD60). Macroscopic assessments indicated dose-related reductions in body weight, ovarian weight, and ovarian length at both postnatal stages in females. Qualitative fluorescence microscopy using rhodamine-labeled PS-NPs revealed dose-related fluorescent signals within the follicular and stromal compartments of the ovary at PD30 and PD60, supporting particle localization in ovarian tissue. Histological and morphometric analyses revealed a reduction in pre-antral follicle numbers at PD30, progressive thinning of the granulosa layer, and a decreased parenchyma-to-stroma ratio, particularly in high-dose offspring. Biochemical analyses indicated oxidative imbalance, characterized by an elevated total oxidant status (TOS) and oxidative stress index (OSI) at PD30, along with a reduced total antioxidant capacity (TAC) and higher oxidative indices at PD60. Endocrine evaluation at PD60 showed dose-related decreases in circulating estradiol and progesterone levels. Immunohistochemical analysis demonstrated increased P53 immunoreactivity and reduced BCL-2 expression, consistent with apoptosis-related signaling in ovarian tissue. Collectively, these findings suggest that lactational exposure to PS-NPs is associated with dose-related ovarian alterations accompanied by oxidative imbalance, endocrine disruption, particle localization, and apoptosis-associated responses, highlighting lactation as a potentially sensitive postnatal exposure window. - Source: PubMed
Publication date: 2026/06/12
Boostanifard MohammadMoradi Hamid RezaAbbasi SajjadKhaksar Zabihollah - Breast cancer (BC) is the most prevalent cancer among women and the second leading cause of cancer-related deaths globally, after lung cancer. Despite advances in treatment, BC remains a major contributor to cancer mortality worldwide, underscoring the need for innovative therapeutic approaches. The TopBP1 (DNA Topoisomerase II Binding Protein 1) gene, involved in DNA damage response and cell cycle regulation, has been associated with cancer progression and resistance to chemotherapy. This study investigates the potential of using CRISPR/Cas9 technology to knockout the TopBP1 gene as a novel strategy in breast cancer research. - Source: PubMed
Publication date: 2026/06/12
Taheri SamaneAzarpira NegarMahmoodi ShirinGila FatemehDara Mahintaj - Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) is a progressive liver disorder driven by high-fat diet (HFD)-induced metabolic stress, oxidative damage, inflammation, and apoptosis. This study investigated the hepatoprotective effects of vitexin (VX) and vitexin-loaded phytosomal nanoparticles (VX-PHY) in HFD-fed rats. Sixty male albino rats were randomly assigned to six groups: standard diet control, standard diet + VX, standard diet + VX-PHY, HFD only, HFD + VX, and HFD + VX-PHY. HFD feeding caused significant weight gain, elevated liver and fat indices, disrupted serum proteins, impaired liver function, and dysregulated lipid profiles. At the molecular level, HFD induced oxidative stress, depleting GSH and antioxidant enzymes while activating the Nrf2/HO-1 pathway. It also triggered hepatic inflammation via NF-κB/COX-2 signaling, increasing TNF-α, IL-1β, and IL-6, and promoted apoptosis by upregulating BAX, Caspase-3, Caspase-8, and downregulating BCL2. HFD additionally activated the PI3K/AKT/mTOR/SREBP-1c axis, enhancing AKT/mTOR phosphorylation, nuclear SREBP-1c, and lipogenic gene expression (FASN, ACC), contributing to hepatic lipid accumulation, which was effectively suppressed by VX-PHY, highlighting its superior anti-lipogenic effect compared with crude VX. VX-PHY co-treatment further enhanced antioxidant defenses, modulated Nrf2/HO-1, suppressed NF-κB/COX-2-mediated inflammation, and attenuated pro-apoptotic signaling, restoring these pathways to near-control levels. Histopathological and ultrastructural analyses confirmed reduced steatosis, hepatocyte ballooning, necrosis, and organelle damage in VX-PHY-treated rats. Overall, vitexin, particularly when delivered via phytosomal nanoparticles, exerts potent hepatoprotective effects in HFD-induced MASLD by simultaneously mitigating oxidative stress, inflammation, apoptosis, and lipid dysregulation via inhibition of PI3K/AKT/mTOR/SREBP-1c, highlighting the therapeutic potential of nanoparticle-based delivery for natural compounds like vitexin. - Source: PubMed
Publication date: 2026/06/12
Hegazy Ahmed MsAl-Ghafari Ayat BDoghaither Huda A AlElmorsy Ekramy MGhaith Mazen MAlshammari Ahmad NajemAlfayoumi Mohamed GHassan Abeer M E - Evasion of apoptosis is a hallmark of cancer. Deregulation of BCL-XL, a member of the BCL-2 family of proteins, has been linked to the development of various tumor types. This study presents the design and synthesis of BCL-XL inhibitors with novel mono- and bicyclic cores. The new structural features were optimized to combine high binding efficiency with the opening of diverse novel vectors for additional modifications. The lead compounds exhibited picomolar affinities and significant cellular potency in the BCL-XL-dependent MOLT-4 cell line, which also translated into marked tumor growth inhibition in a xenograft study. These findings highlight the potential of BCL-XL inhibitors as therapeutic agents in cancer treatment by targeting the apoptotic intrinsic pathway. - Source: PubMed
Publication date: 2026/06/12
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