Ask about this productRelated genes to: EPHX1 Blocking Peptide
- 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 Blocking Peptide
Related articles to: EPHX1 Blocking Peptide
- Hydrolytic drug-metabolizing enzymes (hydrolases) are essential for the metabolism of many therapeutic agents; however, comprehensive data on their tissue distribution and interspecies variability remain limited. To address this knowledge gap, the primary objective of this study was to quantify the abundance of drug metabolism-relevant hydrolases (e.g., CES1/2, PON1/2/3, BPHL, APEH, CMBL, EPHX1/2, DPP4, and AADAC) across liver, intestine, and kidney tissues in humans, rats, mice, dogs, and monkeys using a comprehensive global proteomics approach. Further, we present here qualitative and quantitative differences in intertissue and interspecies variability among 182 detected hydrolases. Humans exhibited the greatest variability of hydrolases across tissues, with marked qualitative and quantitative differences in protein abundance observed between species. Orthology analysis highlighted substantial sequence conservation in monkeys but greater divergence in rodents and dogs. Overall, these findings could provide critical quantitative data to inform animal model selection and improve the translation of preclinical drug metabolism studies to humans for drugs that are majorly metabolized by hydrolases. - Source: PubMed
Publication date: 2026/06/24
Subash SandhyaAhire DeepakJones Robert SMa BinTian YuWang TingKhojasteh S CyrusMurray Bernard PStresser David MTaub MitchellPrasad Bhagwat - Herb-Drug Interactions (HDIs) are a major clinical concern, as they may alter drug efficacy or cause toxicity. This study evaluated the potential HDIs of Echinacea purpurea, Thymus vulgaris, and Salvia officinalis by assessing their effects on Drug-Metabolizing Enzyme (DME) gene expression in rats. - Source: PubMed
Publication date: 2026/05/22
Ahmed Shahira HNaguib Mohamed MSeoudi Dina MEl-Sayed Wael M - BackgroundAlzheimer's disease (AD) involves interactions among genetic, environmental, and lifestyle factors, yet the contribution of environmental exposures to cognitive decline and biomarker changes remains unclear. Detoxification genes such as EPHX1 may influence susceptibility to environmental neurotoxicants.ObjectiveTo evaluate associations between environmental risk, cognitive outcomes, and AD biomarkers, and to examine potential contributions of detoxification genes.MethodsWe analyzed 5101 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) across four study phases. Environmental exposure was summarized using a composite Environmental Risk Score (ERS) derived from Rural-Urban Continuum Codes, Rural-Urban Commuting Area codes, Risk-Screening Environmental Indicators, and occupational exposure. Cognitive outcomes included Mini-Mental State Examination, Clinical Dementia Rating, Montreal Cognitive Assessment, Neuropsychological Test Battery, Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog), and Executive Dysfunction Cognitive Assessment. Biomarkers included PET amyloid/tau, MRI hippocampal volume, and cerebrospinal fluid amyloid-β, tau, and neurofilament light chain. Multivariable regression models adjusted for sociodemographic factors and ε4 carrier status.ResultsERS was significantly associated with CDR (β = -1.13E-07; 95% CI -1.98E-07, -2.75E-08; p = 0.00956) but not with other cognitive measures. EPHX1 showed a significant main effect on ADAS-Cog (β = 0.479; 95% CI 0.0305, 0.927; p = 0.0356). ERS × gene interaction terms were not significant. ERS was not associated with amyloid PET SUVR.ConclusionsEnvironmental risk showed limited associations with AD-related outcomes, while EPHX1 demonstrated a significant main effect on cognitive performance. Longitudinal studies are needed to clarify mechanisms linking environmental exposure and AD. - Source: PubMed
Publication date: 2026/05/25
Kanani KhushiRamakrishnan PrevenaNeupane SnabuMisra ManaliBalmer-Brown KaitlynnHalteman SarahWarrick Tia - 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