Ask about this productRelated genes to: GPX3 antibody
- Gene:
- GPX3 NIH gene
- Name:
- glutathione peroxidase 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-03
- Date modifiied:
- 2015-08-28
Related products to: GPX3 antibody
Related articles to: GPX3 antibody
- Rheumatoid arthritis (RA) is a chronic autoimmune disorder marked by progressive joint destruction and functional impairment. Increasing data indicate that glutamate metabolism is critically involved in RA pathogenesis. This analysis aimed to identify glutamate metabolism-related biomarkers and potential RA therapeutics. - Source: PubMed
Publication date: 2026/04/29
Zhu BingruiLi BaoliangZhang ShuxuQi WenzhuoMu ZhouKong PengHan YingguangShi Zhigang - Colorectal cancer (CRC) is a major cause of cancer morbidity and mortality worldwide, and its progression is closely associated with redox imbalance. The biological role and upstream regulation of the antioxidant enzyme glutathione peroxidase 3 (GPx3) remain poorly understood in CRC. This study integrated analyses from clinical CRC tissues, in vitro functional experiments, molecular biology assays, and public The Cancer Genome Atlas datasets. Techniques included gene expression profiling, -methyladenosine methylation analysis, mitochondrial reactive oxygen species detection, lipophagy assays, lipid droplet staining, transcriptomic and proteomic analyses, ferroptosis sensitivity testing, and in vivo xenograft and metastasis models to investigate the role and underlying mechanisms of GPx3 in CRC. In addition, lung metastatic burden was assessed using in vivo bioluminescence imaging and high-resolution micro-computed-tomography scanning. GPx3 was substantially down-regulated in CRC tissues and cells, primarily due to -methyladenosine modification catalyzed by methyltransferase-like protein 3 (METTL3) and METTL14. Down-regulation of GPx3 expression elevated mitochondrial reactive oxygen species, impaired lipophagy flux, and caused excessive lipid droplet accumulation. Multiomics analyses identified Dickkopf-1 (DKK1) as a downstream target negatively regulated by GPx3 through reactive-oxygen-species-dependent β-catenin signaling. The GPx3-DKK1-solute carrier family 7 member 11 (SLC7A11) axis modulated lipid peroxidation and influenced ferroptosis sensitivity. In vivo xenograft and metastatic models showed that GPx3 suppressed tumor growth and metastasis, and these effects were partially reversed by DKK1. This study demonstrates that METTL3/14-mediated -methyladenosine modification is a key upstream mechanism leading to GPx3 down-regulation in CRC. Down-regulation of GPx3 expression promotes malignant progression by increasing mitochondrial oxidative stress, disrupting lipophagy, and cooperating with the DKK1-SLC7A11 pathway to reduce ferroptosis sensitivity. Targeting this regulatory axis may provide promising molecular strategies for CRC diagnosis and therapy. - Source: PubMed
Publication date: 2026/05/11
Wang HuiyaJin YingyingDong ZiyiHao JieGao ZhanhuaChen ChongYang JiayuWang XinyiYang FangZhang MiaoQiu MinghanLiu HuiGuo YaoyangTian MengranPan ZhanyuZhang XipengGao MingBa YiHu DongzhiZhang MingqingJiang ZhanshengZhang Haiyang - The incidence of papillary thyroid carcinoma (PTC) is constantly increasing in the global population, with no systematic screening. The current challenge is to define relevant risk factors contributing to this increase and to facilitate an early diagnosis. Selenium (Se) is an essential trace element required for proper thyroid function. Selenium deficiency has been associated with papillary thyroid carcinoma, but a comparison of different biomarkers of Se status is missing. Plasma samples of patients and controls were analyzed for three markers of Se status: total plasma Se by total reflection X-ray fluorescence, selenoprotein P (SELENOP) by ELISA, and activity of glutathione peroxidase 3 (GPX3) by enzyme assays. Total plasma Se and GPX3 were significantly lower in patients than in controls (78.1 ± 16.7 µg/L vs. 94.7 ± 19.5 µg/L, P < 0.0001, and 200.6 ± 42.7 U/L vs. 239.2 ± 36.7 U/L, P < 0.0001, respectively). All plasma biomarkers showed significant positive correlations, supporting sample integrity, analytical quality and insufficient Se status. A predictive model was deduced, indicating a significant association between low plasma Se and PTC (OR=5.02, 95%; CI:1.51-16.73; P = 0.009). The results support the hypothesis that Se status is affected by thyroid cancer, that thyroid cancer risk increases in case of Se deficiency, or that the interrelationship is interconnected. As Se deficiency is an addressable health risk, longitudinal studies are required to elucidate the direction of interaction and for testing protective measures. - Source: PubMed
Publication date: 2026/05/07
Tani Latifa Sarra KaziDennouni-Medjati NouriaMedjahedi AbdelkaderRahou ZoubidaBensnane MeriemDali-Sahi MajdaHarek YahiaSun QianHackler JulianSchomburg LutzCharlet Laurent - : Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most consumed drugs worldwide and the main cause of drug hypersensitivity reactions (HSRs). The most common NSAID-HSR class is cross-hypersensitivity (CR), with patients reacting to NSAIDs from different chemical groups without specific immunological recognition, with NSAID-induced acute urticaria/angioedema (NIUA) being the most frequent clinical phenotype. Although CR-HSRs are triggered by arachidonic acid (AA) alterations following cyclooxygenase (COX)-1 inhibition and cysteinyl-leukotrienes synthesis by 5-lypoxygenase (5-LO), current evidence supports the participation of additional mechanisms. As COX-1 and 5-LO head oxidative pathways, it is conceivable that enzymes participating in antioxidant control are involved in these mechanisms. In addition, as the CR-HSR susceptibility seems to be influenced by genetic factors, the possibility of genetic variants playing a role in such enzymes should not be excluded. In this observational case-control study, we analysed for the first time in NIUA the overall genetic variability in key antioxidant defence enzymes genes, including catalase (), glutathione peroxidase ()- and , and superoxide dismutase (). We selected a set of tagging single nucleotide polymorphisms (tSNPs) in these genes using data from Europeans in the 1000 Genomes Project. Two independent Spanish populations (discovery and replication) of NIUA patients and NSAID-tolerant individuals were included. : Twenty-six tSNPs were genotyped in the discovery population, with three that were significantly associated with NIUA: rs3448 (GPX-1), rs3792798 (GPX-3), and rs10432782 (SOD-1). They were then genotyped in the replication group, with rs3792798 being protective and rs10432782 being associated with an increased NIUA risk. : Our results suggest that a role for antioxidant enzyme polymorphisms in NIUA is required. Nevertheless, further research is needed to replicate our findings in other populations and their meaning at the molecular level and to investigate the role of such variants in other CR-HSR-induced phenotypes. - Source: PubMed
Publication date: 2026/03/24
Jiménez-Sánchez Isabel MJurado-Escobar RaquelTriano-Cornejo JoséSáenz de Santa María RocíoNúñez RafaelAllali-Bouamara ImaneRaya-López VictoriaChacón PedroLaguna José JTorres María JDoña InmaculadaCornejo-García José A - Keratoconus (KC) is a common eye disease characterized by progressive corneal thinning and steepening. Despite multiple treatment options, there is no definitive cure for KC. Previously we identified loss and dysregulation of nuclear factor erythroid 2-related factor 2 (NRF2) mediated antioxidant functions in stromal cells and extracellular matrix (ECM) in KC. Here we used tear fluid samples and cell culture models to investigate oxidative stress in KC. - Source: PubMed
Koduri Madhuri ACharter MackenzieSonar RohiniDeshmukh RashmiPrescott Christina RMandel RoseSperber LaurenceLee Ting-FangKahan Elias HHaberman Ilyse DSingh VivekBlitzer Andrea LMaiti GeorgeChakravarti Shukti