PRDX1 Mouse Monoclonal Antibody
- Known as:
- PRDX1 Mouse Monoclonal Antibody
- Catalog number:
- CJC-005052-M02
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- PRDX1 Mouse Monoclonal Antibody
Related genes to: PRDX1 Mouse Monoclonal Antibody
- Gene:
- PRDX1 NIH gene
- Name:
- peroxiredoxin 1
- Previous symbol:
- PAGA
- Synonyms:
- NKEFA
- Chromosome:
- 1p34.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-01
- Date modifiied:
- 2014-11-19
Related products to: PRDX1 Mouse Monoclonal Antibody
Related articles to: PRDX1 Mouse Monoclonal Antibody
- Pathological cardiac hypertrophy is a key risk factor for heart failure (HF). Illustrating the pathogenesis of cardiac hypertrophy may contribute to the treatment of HF. Studies have emphasized that protein ubiquitination is a critical event in HF. In this study, we investigated the role of an E3 ubiquitin ligase, RNF123, in HF induced by angiotensin II (Ang II) infusion and transverse aortic constriction (TAC) surgery. - Source: PubMed
Wang QinyanGuo XiaochenXu JiachenQian JinfuYu TianxiangZheng QingsongWang MengyangLuo WuLiang Guang - Microglia are key regulators of neuroinflammation and neuronal survival after ischemic stroke. Emerging single-cell, transcriptomic, and metabolic studies show that ischemia induces rapid microglial reprogramming toward pro-inflammatory states that exacerbate neuronal death, oxidative stress, blood-brain barrier (BBB) disruption, and white-matter injury. Multiple pathways, including TLR4/NF-κB, NLRP3 inflammasome activation, Notch1-JAK/STAT signaling, epigenetic modulators such as HDAC3 and METTL14, and metabolic shifts involving AMPK/mTOR/HIF1α, collectively shape post-stroke microglial polarization. High-altitude hypoxia elicits similar inflammatory responses, activating microglia through RAGE-MAPK/NFκB signaling, CX3CL1/CX3CR1-dependent synaptic pruning, mitochondrial dysfunction, and lactate-mediated chromatin changes, highlighting hypoxia as a convergent driver of neuroinflammation. Modulating microglial activity, therefore, represents a promising therapeutic strategy. A wide range of natural compounds (e.g., curcumin, acteoside, astagaloside IV, artemisinin), synthetic agents (e.g., DBZ, resolvin D1), and cellular/molecular cellular interventions (e.g., rhFGF21, S100A9 inhibition, RBM3 induction) have shown efficacy in reducing inflammation, preserving BBB integrity, improving mitochondrial function, and promoting M2-like reparative phenotypes in preclinical models. Advances in understanding microglial subtypes, including CH25H, OASL, CD11c, and antioxidant Prdx1-enriched populations, further highlight their dynamic roles across injury and repair. This review presents current insights into microglial signalling, epigenetic and metabolic regulation, and therapeutic targeting in ischemic stroke, integrating parallel insights from high-altitude hypoxia. Together, these prospectives illuminate microglia as crucial mediators of neurovascular injury and recovery, and highlight opportunities for translating microglia-directed therapies into clinical interventions. - Source: PubMed
Publication date: 2026/05/06
Khan ShafaSultan ArmiyaSadik MohdAshraf Mohammad Zahid - Disulfidptosis is a recently discovered mechanism of cell death caused by disulfide stress. Arachidonic acid metabolism (AAM) is one of the metabolic mechanisms of polyunsaturated fatty acids. However, few studies have explored the relationship between disulfidptosis and AAM and how together they affect breast cancer prognosis. The aim of this study was to establish a prognostic model of disulfidptosis and arachidonic acid metabolism in breast cancer and to investigate the potential mechanisms of disulfidptosis and arachidonic acid in breast cancer. - Source: PubMed
Publication date: 2026/05/07
Yan TaoYu BolinQian FengyuanFang LinZhao YuanyuanYe Danrong - Hydrogen peroxide (HO) plays a dual role as both a signalling molecule and a mediator of oxidative stress. Although mitochondria are major producers of HO, the relative contributions of mitochondrial versus cytosolic antioxidant systems to mitochondrial HO homeostasis in intact cells remain poorly defined. Here, we combined compartment-resolved live-cell imaging using HyPer7, inducible mitochondrial HO generation (matrix-targeted d-amino acid oxidase), kinetic modelling, and a targeted CRISPR/Cas9 screen to dissect determinants of mitochondrial HO dynamics in HEK293 cells. Unexpectedly, we found that the cytosolic peroxiredoxin PRDX1 is a dominant regulator of mitochondrial matrix HO levels. Loss of cytosolic PRDXs markedly enhanced matrix Hyper7 signals under both exogenous and mitochondria-intrinsic HO production, exceeding the effects of deleting mitochondrial peroxiredoxins. Modelling and transport experiments indicated a very high permeability of the mitochondrial inner membrane to HO enabling rapid efflux and the establishment of steep concentration gradients. This permits the cytosol to function as a major sink to limit matrix HO accumulation. PRDX1 deficiency sensitized cells to chronic mitochondrial oxidative stress. A targeted CRISPR screen identified the Rab7 GAP TBC1D5, linking mitophagy to cellular survival under these conditions. Consistently, PRDX1/2-deficient cells exhibited elevated mitophagic flux, indicating mitochondrial quality control as a compensatory response. Our study reveals that cytosolic PRDXs critically impact mitochondrial redox homeostasis and provides a systems-level framework for understanding compartmental redox control and stress adaptation. - Source: PubMed
Publication date: 2026/04/30
Jacobs Lianne JhcDoll SebastianTrümbach DietrichVeronese MatteoDi Pietro GiadaYapici Fatma IsilHasberg LidwinaGentzsch PascalGerlich SarahHansen Jensvon Karstedt SilviaRugarli Elena IConrad MarcusSalvador ArmindoRiemer Jan - Renal cell carcinoma (RCC) is a highly heterogeneous malignant tumor, characterized by a globally increasing incidence and mortality rate. Although surgical resection serves as the standard treatment for localized RCC, recurrence and metastasis remain major clinical challenges. Based on patient sample analysis and signaling pathway investigation, the present study identifies peroxiredoxin 1 (PRDX1) as a potential therapeutic target for RCC. - Source: PubMed
Publication date: 2026/04/17
Liang ZhiLin XiaochunZeng ShenWu LiliDong YujunZhang ChenLi MeiZhu FudiChen LuNi Suiqin