Ask about this productRelated genes to: PRDX1 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 antibody
Related articles to: PRDX1 antibody
- Oxidative stress is a primary mediator of male reproductive decline and offspring behavioral abnormalities. Unlike females, males exhibit enhanced antioxidant capacity and sustained fertility, but the mechanism is unclear. Here, using single-cell transcriptomics and cross-sex comparisons, we identify Grtp1 as critical for counteracting male reproductive aging and protecting offspring from behavioral deficits by preserving germline redox homeostasis and sperm DNA methylation stability. Grtp1 ablation recapitulates aging phenotypes, including oxidative stress, mitochondrial dysfunction, impaired spermatogenesis, and offspring anxiety and social deficits. Mechanistically, GRTP1 interacts with PRDX1/4 and TXN to maintain germline redox balance. Notably, growth hormone treatment in aged males rescues germline redox homeostasis, restores abnormal sperm DNA methylation and quality, and ameliorates offspring behavioral deficits in a Grtp1-dependent manner. Our study establishes GRTP1 as a key redox safeguard against male germline aging and highlights the GH-GRTP1 axis as a promising therapeutic target for age-related reproductive and intergenerational behavioral deficit. - Source: PubMed
Publication date: 2026/09/27
Liu YingdongLiu ShanyaoLiang HaixinYang JianiLi YanheYin JiqingZhang XueguangZhang YanBai DandanYan ZihuiZhang ZhuoaoJia YanpingLiu KuishengSheng YifanXiang JianiXi ChenxiangDong BaoxingLei XinyiChen JiayuWang HongGuo YiZhang YanpingGao ShaorongLiu Wenqiang - The oviduct provides an optimal environment to protect gametes and embryos against oxidative stress, yet its endogenous defenses remain insufficiently characterized. This study examined the expression and the spatial, temporal and hormonal regulation of four major antioxidant enzyme families - peroxiredoxins (PRDX), catalase (CAT), superoxide dismutases (SOD), and glutathione peroxidases (GPX) - in the bovine oviduct. Oviducts from cyclic cows were analyzed in three complementary experiments. In vivo (Experiment 1), mRNA expression of antioxidant enzymes (CAT, GPX1-3, PRDX1-6, SOD1-2) was compared between oviductal regions (ampulla vs. isthmus) and estrous cycle stages (pre-ovulatory, post-ovulatory, luteal). In vitro (Experiment 2), physiological concentrations of progesterone (100 ng/mL) and estradiol (300 pg/mL) were tested on gene expression in ampullary and isthmic epithelial spheroids. In Experiment 3, GPX protein abundance and enzymatic activity were assessed in oviductal fluid. All transcripts were detected in the oviduct epithelium. GPX1-3 and PRDX6 showed region-specific expression, with GPX1-2 enriched in the ampulla and GPX3 and PRDX6 in the isthmus. Stage-dependent variations were observed for CAT, SOD2, PRDX2, PRDX4, and PRDX6 in a region-dependent manner. Progesterone upregulated GPX2 and PRDX6 in both ampullary and isthmic spheroids, while estradiol selectively stimulated PRDX4 expression in isthmic spheroids. GPX3 protein abundance decreased at the post-ovulatory stage, in both regions, and mirrored the GPX activity in the oviduct fluid. These results demonstrate that antioxidant enzyme expression in the bovine oviduct is dynamically regulated by region, cycle stage, and hormonal milieu, highlighting their role in maintaining redox homeostasis during early reproductive events. - Source: PubMed
Publication date: 2026/09/23
Braga Rachel FerreiraMaia Ana Lucia Rosa E SilvaPereira Paulo Victor Dos SantosDouet CécileCarvalho Anaïs VitorinoMermillod PascalDemattei Marie-VéroniqueSouza-Fabjan Joanna Maria GonçalvesSaint-Dizier Marie - Articular cartilage degeneration is a hallmark of osteoarthritis (OA); however, underlying molecular mechanisms remain poorly understood. Transforming growth factor alpha (TGFα) and chondrocyte metabolism have been independently implicated in OA pathogenesis; in this study, we investigated whether TGFα affects chondrocyte metabolism. - Source: PubMed
Publication date: 2026/09/02
White Emily LDay Emily AAppleton C ThomasGrol Matthew WBeier Frank - Ischemic stroke triggers profound neuroinflammation and autophagic stress, driven predominantly by microglial overactivation. However, effective therapies targeting this pathogenesis remain elusive. Here, we report the use of 3-hydroxydehydroleucodin (3-Hyd), the primary active component from Kudiezi injection used in China for ischemic stroke patients, as a potent neuroprotective agent that markedly reduces the cerebral infarct area and improves neurological deficits in a mouse model of transient middle cerebral artery occlusion (tMCAO). Integrated bulk RNA sequencing and in vitro assays revealed that 3-Hyd significantly suppressed the microglial proinflammatory phenotype and excessive autophagic flux. Mechanistically, through chemical biology approaches, we discovered that 3-Hyd directly binds to the V51 and R128 residues of peroxiredoxin 1 (PRDX1), which physically disrupts the pathological binding of PRDX1 to its E3 ubiquitin ligase TRIM21, thus preventing the polyubiquitination of PRDX1 at the K109 residue and its subsequent proteasome degradation. Consequently, stabilized PRDX1 impedes TRAF6 ubiquitination, effectively blocking the downstream NF-κB signaling cascade. Strikingly, the anti-neuroinflammatory and cerebroprotective effects of 3-Hyd were largely abolished in microglia-specific Prdx1 conditional knockdown (Cx3cr1) mice. Together, our findings elucidate a novel TRIM21-PRDX1-TRAF6 signaling axis that governs microglial homeostasis and highlight the pharmacological stabilization of PRDX1 by 3-Hyd to block the binding of TRIM21 with PRDX1 as a promising therapeutic strategy for ischemic stroke. - Source: PubMed
Publication date: 2026/09/09
Liu KuiWang LingChen ZhuoQiu Yu-XuanGao Jia-HongXie Ting-TingLi YueHuang HeHu YangHu Li-HongPang Tao - Peroxiredoxin 1 (PRDX1) is a highly conserved, thiol-dependent peroxidase that rapidly scavenges reactive oxygen species to modulate redox signaling. PRDX1-null mice exhibited genomic instability, shortened life span, and accelerated tumorigenesis, including development of lymphomas, sarcomas, and carcinomas. Despite extensive characterization of these phenotypes, the molecular mechanism by which PRDX1 loss causes genomic instability remains poorly understood. Here, we show that PRDX1 deficiency alters nucleolar morphology, impairs RNA polymerase I (POL-I)-dependent transcription of pre-ribosomal RNAs, and triggers nucleolar genomic instability. This oxidative stress-induced nucleolar dysfunction promotes the stability of secondary DNA structures, such as RNA-DNA hybrids and G-quadruplex DNA, contributing to nucleolar genomic instability. We demonstrate that PRDX1 loss reduces nascent ribosomal RNA (rRNA) levels and impairs rRNA processing, further affecting ribosome biogenesis. Mechanistically, we established that PRDX1 loss triggers activation of the nucleolar DNA damage response characterized by activation of the DNA repair kinase ATM and elevated TCOF1 within the nucleolus. In addition, we observed recruitment of the MRE11-RAD50-NBS1 (MRN) complex subunit NBS1 to ribosomal DNA (rDNA) loci and this was further increased under oxidative stress. NBS1 accumulation correlates with the repression of rDNA transcription by POL-I, potentially delaying rRNA synthesis, and safeguarding the nucleolar genome from further oxidative damage. Collectively, these findings uncover a previously unrecognized, but critical role, for PRDX1 in maintaining nucleolar integrity and ribosomal biogenesis through redox-dependent regulation of rDNA transcription and processing machinery. - Source: PubMed
Publication date: 2026/09/09
Gujar VaibhaviFurusawa TakashiSharma ShaluBoateng FrimpongLi HaojianAchour CyrinneTaniyama DaikiKruhlak MichaelPommier YvesOberdoerffer ShaliniStracker Travis HWeyemi Urbain