Nrf2 Polyclonal pAb
- Known as:
- Nrf2 Polyclonal pAb
- Catalog number:
- ASAKAP-TF125D
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Nrf2 Polyclonal pAb
Related genes to: Nrf2 Polyclonal pAb
- Gene:
- KEAP1 NIH gene
- Name:
- kelch like ECH associated protein 1
- Previous symbol:
- -
- Synonyms:
- KIAA0132, MGC10630, MGC1114, MGC20887, MGC4407, MGC9454, INrf2, KLHL19
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-30
- Date modifiied:
- 2015-11-23
Related products to: Nrf2 Polyclonal pAb
Related articles to: Nrf2 Polyclonal pAb
- Oxeiptosis is a form of regulated cell death that is independent of caspases and is generally considered to be non-inflammatory. This process is triggered by reactive oxygen species and involves the Kelch-like ECH-associated protein 1 (KEAP1)-phosphoglycerate mutase family member 5 (PGAM5)-apoptosis-inducing factor mitochondria-associated 1 (AIFM1) signaling pathway. This review critically assesses the potential of oxeiptosis-related molecules and multi-omics signatures as biomarkers in human cancers, highlighting their analytical validity and future perspectives in the field of translational laboratory medicine. Other factors, such as KEAP1, PGAM5, and AIFM1, are not unique to oxeiptosis but are also involved in the regulation of other forms of cell death, including antioxidant signaling, mitophagy, and apoptosis. Concurrently, AIFM1 may need to be dephosphorylated at serine 116 (Ser116), PGAM5 must be activated, oxidative stress is required, and there must be no activation of caspases, although this pathway profile is not analytically validated. While many composite signatures exhibit hypothesis-generating potential for prognostic stratification, molecular subtyping, and prediction of therapeutic responsiveness, most have not yet been prospectively validated and are at risk of data set overlap, overfitting, algorithm instability, and poor inter-cohort transportability. Preanalytical variability, specimen stability, assay standardization, normalization, inter-platform concordance, and undefined clinical performance thresholds are other factors that limit translation. In summary, the current state of oxeiptosis-related biomarkers is not clinically validated and has a low level of translational readiness. To achieve future progress, standardized definitions of analytic measures, multicenter validation, and prospective clinical utility must be demonstrated. - Source: PubMed
Publication date: 2026/06/20
Khan AbidaAlruwaili Mohammed MAlhuthali Hayaa MAlzahrani ShathaAlrehaili Amani AAlshammari AbdulkarimSiddique Muhammad IrfanImran Mohd - Major depressive disorder (MDD) represents a serious psychiatric condition with limited treatment options. Targeting microglial inflammation and the associated oxidative stress represents a promising therapeutic strategy for MDD. In this study, 33 novel febuxostat derivatives were designed and synthesized by conjugating the febuxostat core with various 1,2,3-triazole moieties via click reaction. All synthesized compounds were evaluated for their anti-inflammatory activity in LPS-stimulated BV-2 microglial cells. Among them, Compound 6i and 6j emerged as the most potent candidate, significantly suppressing NO production (IC values of 5.90 ± 0.16 μM and 3.45 ± 0.18 μM, respectively), pro-inflammatory cytokines IL-1β, IL-6, TNF-α, and the upstream inflammatory enzymes COX-2 and iNOS expression without cytotoxicity. Mechanistic studies revealed that compounds 6i and 6j activated the Nrf2-HO-1 pathway, attenuated ROS accumulation, and restored GSH levels and SOD activity. Molecular docking further revealed that compounds 6i and 6j bind strongly to Keap1 with binding energies, suggesting that they prevent Nrf2 degradation by occupying the Keap1 binding pocket. In vivo, compound 6j ameliorated LPS-induced depressive-like behavior in mice, concomitant with reduced microglial/astrocytic activation and decreased IL-1β/TNF-α mRNA expression in the hippocampus. These findings suggest that compound 6j exerts antidepressant-like effects through Nrf2-HO-1-mediated antioxidant and anti-inflammatory mechanisms, representing a promising lead compound for MDD treatment. - Source: PubMed
Publication date: 2026/06/17
Wang LanHou XixiLiang XuSong MingxuanYan DongZhang QingqingWang YimianGao EnGao MenglongLi MengyuanGuo JingjingMao LongfeiLi Sanqiang - Alzheimer's disease (AD) is a severe neurodegenerative disorder. With current therapies failing to halt clinical progression, identifying novel disease-modifying therapeutics is of paramount urgency. Although ferroptosis has emerged as a crucial driver of AD pathogenesis, effective pharmacological strategies targeting this pathway remain limited. Bioinformatic analysis revealed close associations among ferroptosis, oxidative stress, the Keap1-Nrf2 pathway, and AD. Compound 4-95, a selective Keap1-Nrf2 protein-protein interaction (PPI) inhibitor, significantly alleviated Erastin and RSL-3-induced ferroptosis in SH-SY5Y and HT-22 cells. In Aβ-treated cell models, 4-95 dose-dependently decreased Aβ and p-Tau expression, while increasing the anti-ferroptotic proteins GPX4 and SLC7A11. Keap1 and GPX4 knockdown verified that 4-95 inhibits ferroptosis via the Keap1-Nrf2-GPX4 axis. In vivo, 4-95 markedly improved cognitive and spatial memory deficits in Aβ-induced AD mice, promoted Nrf2 nuclear translocation, upregulated the downstream antioxidant targets HO-1 and NQO1, and attenuated neuronal injury. Collectively, the study reveals a new mechanism of a Keap1-Nrf2 PPI inhibitor that mitigates AD pathogenesis by directly inhibiting ferroptosis. This novel mechanism underscores a new class of disease-modifying candidates for AD treatment, representing a new therapeutic strategy for this devastating disorder. - Source: PubMed
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Publication date: 2026/06/17
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