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
- Morin (3,5,7,2',4'-pentahydroxyflavone) is a dietary flavonol with broad neuroprotective, anti-inflammatory, and antioxidant actions across central and peripheral nervous system models. This synthesis consolidates evidence from in vitro and rodent studies-covering neurodegenerative proteinopathies (Alzheimer's, Parkinson's, and Huntington's), neuropathic pain, epilepsy, stress- and schizophrenia-like phenotypes, and chemo-/toxicant-induced neurotoxicity-to evaluate morin's consistent benefits on survival, motor/cognitive performance, and biochemical normalization. Morin mitigated neurotoxicity induced by doxorubicin, ifosfamide, vincristine, acrylamide, heavy metals, and endocrine disruptors. Context-specific effects included modulation of disease-defining pathways (GSK3β/CDK5, mTORC1, PARP, and AMPK-ULK1-TFEB), microglial polarization, and normalization of neurotransmission (dopamine, GABA, 5-HT, and reduced AChE). Core mechanisms included the following: restoration of redox and mitochondrial homeostasis via Nrf2/HO-1 activation; replenishment of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH); decreased reactive oxygen species (ROS), malondialdehyde (MDA), and nitric oxide (NO); and preserved mitochondrial potential/fusion; suppression of innate immune and inflammasome signaling through downregulation of TLR4/NF-κB and ERK-p65, reduced TNF-α, IL-1β/IL-6, iNOS/COX-2; inhibition of NLRP3/caspase-1; and rebalancing of cell-death programs (↓Bax/caspase-3, ↑Bcl-2; attenuation of RIPK1/RIPK3/MLKL-mediated necroptosis). Formulation strategies (intranasal microemulsions, pluronic micelles, and more soluble derivatives) have enhanced brain exposure and efficacy, but translation now warrants optimized delivery, pharmacokinetic-pharmacodynamic mapping, target engagement biomarkers, and rigorously controlled trials to define dose, route, and indications as adjunctive to standard care in neurodegeneration, neuropathic pain, and toxicant-related brain injury. Collectively, morin emerges as a multitarget neuroprotective scaffold with reproducible functional and mechanistic benefits. - Source: PubMed
Ekundayo Bidemi EmmanuelEkundayo Motunrayo ComfortAlonge Sunday AyodeleObafemi Blessing AriyoObafemi Tajudeen OlabisiLebelo Sogolo LuckyNtwasa Monde McMillan - Covid-19 pandemic was caused by a novel coronavirus, SARS-CoV-2 and caused a tremendous burden to humans including thousands of deaths. SARS-CoV-2 still causes the respiratory diseases to humans annually. It is known that the pathological outcomes may be different from sexes of humans infected with viral diseases. Here, we studied the pathological difference between females and males infected with the recent SARS-CoV-2 in 6-week-old hACE2-trangenic mouse models. When female and male mice were intranasally infected with the recent SARS-CoV-2/2025, no mortality was observed in both infected female and male mice. However, the infected female mice suffered from more body-weight loss than the infected male mice with higher viral titers in the lungs. The infected male mice produced higher amount of the immune-stimulatory cytokines such as TNF-α and IFN-γ, and anti-apoptotic genes such as BCL2 and Bcl-XL in the lungs than those of the infected female mice. Taken together, it seems that the infected male mice with the recent SARS-CoV-2/2025 could suffer from milder clinical signs than the infected female mice because of the increased expression of immune-enhancing cytokines and anti-apoptotic genes. - Source: PubMed
Publication date: 2026/09/16
Seo HeejeongSeo Sang Heui - Epstein-Barr virus (EBV) BamHI-A rightward frame 1 (BARF1) is a viral oncogene implicated in epithelial malignancies, but the determinants of its transforming activity remain incompletely defined. We generated BARF1 truncation constructs and targeted mutants to examine the contribution of residues 35-38 and adjacent Ser39 in BALB/c 3T3 fibroblasts using serum deprivation, tumorigenicity, BCL-2 expression, and molecular docking assays. Deletion of residues 35-38 in full-length BARF1 reduced viable cell maintenance under severe serum deprivation, whereas Ser39-to-Ala substitution in the BARF1 1-56 background markedly reduced the viable cell advantage of this fragment. Neither mutant produced detectable tumors during the 28-day observation period. Full-length BARF1 induced tumors in all animals, whereas BARF1 1-56 retained partial tumor-forming activity. BARF1 1-46 maintained higher viable cell numbers under serum-limiting conditions but produced no detectable tumors, suggesting a contribution of residues 47-56 to tumor formation. BCL-2 remained detectable in both non-tumor-forming mutants. Exploratory docking predicted a more favorable score and distinct positioning for the wild-type 35-39 peptide relative to the catalytic subunit of cAMP-dependent protein kinase A (PKA) than for the mutant peptides; however, this analysis does not demonstrate Ser39 phosphorylation or PKA-dependent BARF1 activity. Overall, these findings support a functional contribution of the BARF1 region encompassing residues 35-39 to viable cell maintenance under serum deprivation and tumor formation. Because construct-level BARF1 protein abundance, stability, secretion, and localization were not assessed, the observed phenotypes cannot be attributed solely to the altered residues. - Source: PubMed
Publication date: 2026/09/16
Sakka EmnaTaleb KahinaSaoudi BilalZawati ImenSaadi HaneneKhenchouche AbdelhalimBoughalmi MondherSall AlhoussenouHouali Karim - Prenatal stress (PS) is a recognized risk factor contributing to the development of depressive-like behaviors in offspring. Naringin (NRG), a bioactive flavonoid abundant in citrus fruits, exhibits notable antidepressant and neuroprotective properties. This study aimed to elucidate the molecular mechanisms underlying NRG's effects in PS offspring, focusing on IRE1/XBP1 pathway of endoplasmic reticulum stress (ERS). The results demonstrated that NRG treatment significantly alleviated depressive-like behavior and attenuated hippocampal neuronal damage in PS offspring rats. Integrative network pharmacology and molecular docking analyses predicted that NRG may interact with ERS-related proteins (GRP78, CHOP, IRE1, XBP1). Consistently, PS exposure elevated the expression of GRP78, CHOP, p-IRE1, XBP1s, Bax, and Caspase-12 while decreasing Bcl-2, triggering ERS-mediated neuronal apoptosis. NRG treatment effectively reversed these molecular alterations and suppressed apoptosis. Strong correlations were observed between behavioral improvements and the downregulation of IRE1/XBP1 pathway components and apoptotic markers. In conclusion, NRG exerts antidepressant-like effects in PS-exposed offspring likely by suppressing hippocampal ERS via the IRE1/XBP1 pathway, thereby reducing neuronal apoptosis. These findings position NRG as a promising candidate for novel antidepressant therapeutics. - Source: PubMed
Publication date: 2026/09/16
Gong ZhengWang YanniDi DandanZhu TongZhao Hui - Endocrine-disrupting chemicals (EDCs), including di(2-ethylhexyl) phthalate (DEHP) and propylparaben (PrP), are widespread environmental contaminants with adverse effects on reproductive health. However, the mechanisms underlying their sex-specific toxicity, particularly under combined exposure, remain incompletely understood. In this study, experimental toxicology was integrated with network-based analyses to investigate the reproductive toxicity of DEHP and PrP in Japanese medaka (Oryzias latipes), with particular emphasis on the brain-gonad-liver axis. Following 28 days of exposure, DEHP exposure reduced the gonadosomatic index (GSI) by 60.45% and increased gonadal 17β-estradiol (E) and testosterone (T) levels to 203.57 pg/g and by 2.39-fold for females, respectively (p < 0.05). In males, DEHP exposure increased gonadal E and T concentrations to 87.52 and 38.73 pg/g, respectively, whereas combined exposure increased hepatic VTG levels by 1.37-fold. In contrast, hepatic VTG concentrations decreased by 735.45 ng/g in DEHP-exposed females (p < 0.05). Network toxicology analysis identified PTGS2, BCL2, EGFR, ESR1, and IL10 as major DEHP-associated targets, whereas PrP was predicted to affect AKT1 and STAT3 through the EGFR tyrosine kinase inhibitor resistance pathway. Alterations in hormone levels and gene expression across the brain, gonads, and liver indicated systemic dysregulation of the hypothalamic-pituitary-gonadal axis. Despite their distinct molecular targets, DEHP and PrP converged on shared pathways, including chemical carcinogenesis-receptor activation and PI3K/Akt signaling. These findings demonstrate sex-specific disruption of the brain-gonad-liver axis by DEHP and PrP and highlight the importance of considering combined EDC exposure in reproductive hazard assessment. - Source: PubMed
Publication date: 2026/09/10
Li YunyangZheng NaPan JiaminWang Sujing