Ask about this productRelated genes to: EPHX1 antibody
- Gene:
- EPHX1 NIH gene
- Name:
- epoxide hydrolase 1
- Previous symbol:
- EPHX
- Synonyms:
- -
- Chromosome:
- 1q42.12
- Locus Type:
- gene with protein product
- Date approved:
- 1988-08-09
- Date modifiied:
- 2016-10-05
Related products to: EPHX1 antibody
Related articles to: EPHX1 antibody
- Epoxide hydrolases (EHs) constitute a conserved enzyme family that catalyzes the hydrolysis of epoxides into less reactive diols. Beyond their canonical roles in xenobiotic detoxification, EHs have emerged as critical regulators of lipid metabolism, redox balance, and inflammatory signaling. Accumulating evidence implicates EH family members, particularly Ephx1 (microsomal EH) and Ephx2 (soluble EH), in cardiovascular diseases, cancer, neurodegeneration, metabolic disorders, and other pathological conditions. More recently, studies have uncovered specialized functions of Ephx3 and Ephx4, broadening our understanding of EH biology and highlighting their tissue-specific roles in skin homeostasis and lipid signaling. Here, we systematically review the structural features, catalytic mechanisms, and physiological functions of EHs, with an emphasis on their regulatory networks in human diseases. We further discuss advances in genetic, epigenetic, and translational studies that connect EHs to disease susceptibility and progression. Finally, we evaluate the therapeutic potential and challenges of targeting EHs, particularly soluble EH inhibitors, and propose future research directions to bridge basic discoveries with clinical translation. This review aims to provide a comprehensive framework for understanding the multifaceted roles of EHs and to inspire novel strategies for precision medicine. - Source: PubMed
Publication date: 2026/04/28
Tan YadanXu JingjingHuang ZitengWang XiranXing JinshanLi ShengbiaoYi Jingyan - Although the COVID-19 pandemic has now been down-graded, long COVID (LC) presents an ongoing risk of long-term disease for a significant percentage of the population, even after mild or no symptoms upon infection. LC post-viral effects have been associated with oxidative stress (OS), impacting canonical cell function. The aim of this study was to investigate the association of eight OS-related single nucleotide polymorphisms (SNPs) on LC susceptibility among patients with mild or no symptoms during SARS-CoV-2 infection, with emphasis on a clinically homogeneous population free from bias and overlap with other conditions. Blood samples were collected from 85 clinically confirmed LC patients and 96 unvaccinated controls (observational case control study) all with mild/asymptomatic infection, and analysed by targeted SNP genotyping in the GSTP1, SELENOS, CAT, SOD2, and EPHX1 OS-related genes. Τhe control individuals had been infected at least 6 months prior to enrollment and had not developed any symptoms related to long COVID. Our analysis revealed associations between SOD2 and EPHX1 polymorphisms and disease progression, with pre-existing thyroid disease and acute phase symptoms being significant aggravating factors. Machine Learning (ML) analysis produced a 10-factor predictive model for LC with a balanced accuracy over 0.74, released herein as an open-access LC risk rating webtool. Our findings suggest that individuals' genetic antioxidant capacity may plays an important role in long covid, fitting with current ideas of mitochondrial dysfunction and viral persistence. It is also shown how well diagnosed and bias free cohorts can reveal patterns often missed in self-reported cases and the potential for predictive tools that combine genetic and clinical data. - Source: PubMed
Publication date: 2026/03/26
Katsarou Martha-SpyridoulaPapasavva MariaTsolakou AnniaChristodoulou AvgiAntonoglou ArchontoulaRaptis AthanasiosKontaxakis AntoniosGavrielatos MariosMichalopoulos IoannisVassiliou Alice GStefanatou MariaPappas GeorgiosMoschos Sterghios ADrakoulis NikolaosKatsaounou Paraskevi - Aspergillus flavus infection and the resulting aflatoxin contamination pose serious threats to agricultural commodities, including nutmeg (Myristica fragrans). The use of indigenous yeasts offers a promising biological strategy to suppress A. flavus and reduce aflatoxin levels. This study isolated and characterised yeasts from nutmeg leaves with the ability to decontaminate aflatoxin B1 (AFB1) and inhibit A. flavus. Eight isolates were obtained, among which DAP1 identified as Aureobasidium melanogenum exhibited the strongest activity. DAP1 achieved a 50.4% reduction of AFB1 in vitro, as quantified by HPLC, and inhibited the growth of A. flavus by 43.6% in dual-culture assays. Whole-genome sequencing of DAP1 yielded a 24 Mbp genome with a GC content of 50.14%. Genome annotation revealed putative AFB1 detoxifying genes, including cytochrome P450 monooxygenase (CYP531), glutathione transferase (GST), epoxide hydrolase (EPHX1), and aflatoxin B1 aldehyde reductase (AKR7). AntiSMASH analysis further identified biosynthetic gene clusters showing similarity to bioactive metabolites such as yanuthone (50%), lucilactaene (46%), and choline (100%). In vivo assays using nutmeg seeds confirmed the antagonistic activity of DAP1, which suppressed A. flavus growth by 58.3%. LC-MS/MS analysis showed that AFB1 levels in DAP1-treated seeds were reduced to below 1.26 ppb compared to 20.03 ppb in untreated controls. Overall, these results highlight the biocontrol potential of A. melanogenum DAP1 and its promise as a natural strategy for mitigating aflatoxin contamination in agricultural products. - Source: PubMed
Publication date: 2026/03/05
Harahap IsrawatiMaryam RomsyahSudirman Lisdar IdwanAstuti Rika Indri - Modulation of circadian rhythms impairs homeostasis, resulting in altered susceptibility to disease development. New perspectives on nutrition emphasize the circadian timing of food intake. Here, we found that the ad libitum feeding of oxidized frying oil disrupted the conversion of epoxides to diols in the kidneys, leading to aggravated renal injury. Interestingly, the circadian rhythms of epoxides and their diols in the kidneys and plasma showed differences between the light and dark phases. We demonstrated that time-imposed feeding of fried oil during the active period resulted in limited damage to renal function, conversely, renal function was impaired during the inactive period. Remarkably, feeding with epoxy stearic acid (EpSA) from fried oil during the inactive period disrupted the rhythmicity of epoxide hydrolases and related metabolites, and fueled the progression of renal fibrosis and injury. The effect of EpSA on SMA and E-cadherin, two specific biomarkers for renal inflammation and fibrosis, are lost in knockouts of Ephx1 and Ephx2, which encodes for epoxide hydrolases. In addition, dietary supplementation with linoleic acid, which inhibits epoxide hydrolases, protected mice from damage caused by time-imposed feeding of EpSA. Our findings revealed that the time-of-day dependence of epoxide hydrolases, and circadian disruption induced by time-imposed feeding of EpSA from thermo-induced oxidized oil have adverse effects on kidney function. - Source: PubMed
Publication date: 2026/02/13
Liu YanjunLu MeishanDu YanpengXu JieFan MingjieXue ChanghuLiu Yuanfa - Sheep () tail fat serves as a crucial energy reserve for adapting to harsh environments. However, excessive deposition can reduce farming efficiency and product quality. Elucidating the regulatory mechanisms of tail fat deposition is of great significance for genetic improvement in sheep. - Source: PubMed
Publication date: 2026/01/30
Gao LeiZhang YunyunZhang YiyuanPeng WeifengZhang ZhenliangLiu YuchengWang JingjingWan PengchengZhao Zongsheng