Ask about this productRelated genes to: OPRK1 Blocking Peptide
- Gene:
- OPRK1 NIH gene
- Name:
- opioid receptor kappa 1
- Previous symbol:
- -
- Synonyms:
- KOR, OPRK
- Chromosome:
- 8q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-11
- Date modifiied:
- 2016-10-05
Related products to: OPRK1 Blocking Peptide
Related articles to: OPRK1 Blocking Peptide
- Aberrations in trophoblast proliferation, invasion and hypoxia adaptation are implicated in pregnancy-related complications. OPRK1, encoding the κ-opioid receptor 1, is a member of the G protein-coupled receptors. In this study, we observed a marked downregulation of OPRK1 in decidual-side placental tissue from patients with preeclampsia (PE). Using HTR-8/SVneo trophoblasts, we found that OPRK1 knockdown inhibited cells migration, induced G0/G1 arrest and increased apoptosis, while overexpression reversed these effects. OPRK1 knockdown suppressed PI3K/AKT signaling and epithelial-mesenchymal-transition related pathways. In a L-NAME-induced PE mouse model, the OPRK1 agonist U50488H administration ameliorated PE-related symptoms including hypertension, placental defects, and fetal growth restriction. Therefore, our data indicated that OPRK1 may represent a potential therapeutic target for PE, although further validation in preclinical models is needed. - Source: PubMed
Publication date: 2026/06/08
Yuan YiZeng WeihongSong LinlinQin ChuanmeiZhang YuanWu FanXu YichiLin Yi - Sepsis is a life-threatening condition characterized by infection-induced organ dysfunction, with fluid imbalance and cardiovascular instability as cardinal features. Although circulating procalcitonin (PCT) is widely used as a diagnostic and prognostic marker in sepsis, its pathophysiological role remains poorly understood. Here, we identify a central neural circuit through which PCT directly disrupts fluid homeostasis: systemic PCT crosses the blood-brain barrier, activates calcitonin receptors, and depolarizes the Oprk1-expressing neurons in the ventromedial preoptic nucleus of the hypothalamus (VMPO). In vivo, PCT administration induces polydipsia and polyuria-phenotypes recapitulated by chemogenetic stimulation of VMPO neurons. We demonstrate that VMPO neurons project to and activate arginine vasopressin (AVP)-expressing neurons in the supraoptic nucleus (SON), leading to increased blood pressure. Together, our findings define a PCT-sensitive VMPO→SON neural circuit that integrates fluid balance and cardiovascular regulation. Our data highlight critical role of the brain in coordinating organ pathophysiology during infection. - Source: PubMed
Publication date: 2026/06/11
Lin WeiLiu TingjunHuang JinfengLi LanxiangXu DejiaoLiu TaianLi MengqiMao ZhenWen YiGuo JiajiaLu ZhonghuaBao JinNaumann Robert KWang Hong - The vaginal microbiome is essential for women's health, yet its genomic diversity and interaction with the host remain incompletely characterized. Here we present the Global Vaginal Metagenome-assembled Genomes catalog, an extensive repository of vaginal microbial genomes generated by integrating 10,665 in-house Chinese metagenomes, with 2,967 publicly available metagenomes and 1,433 bacterial isolates. The catalog comprises 65,055 genomes from 890 prokaryotes, 11 eukaryotes and 6,590 viral taxonomic units, many not represented in public reference databases. We investigate virus-bacteria interactions, revealing conserved phages-host associations. We then identify substantial intraspecies genomic and functional variations displaying population-specific patterns. A metagenome-genome-wide association study identifies seven host genetic loci associated with vaginal species at study-wide significance and replicated in at least one independent cohort, notably connecting the gene OPRK1 with the potential pathogen Ureaplasma urealyticum. In summary, our research provides a comprehensive reference for future studies on genotype-phenotype interplay within the human vaginal microbiome. - Source: PubMed
Publication date: 2026/06/11
Jie ZhuyeLiang WeitingDing QiuxiaLiu XiaominZhang YunhongChen NaLi ShenghuiTong XinGao HongqinLu RuikeHuang XinchengGuo RuochunChen JunhongZhu JieZhang ZheLiu NaXie ZhangweiWang XiamanQi LeLi YumeiXiao LiangZhang ShaoqiaoJin XinXu XunYang HuanmingWang JianZhao FangqingJia HuijieKristiansen KarstenZhang TaoHao LilanZhu LanChen Chen - Opioid use disorder (OUD) is caused by a complex interplay between genetic and non-genetic factors. DNA methylation is an epigenetic mechanism that modulates gene expression. Data on DNA methylation and opioid addiction and treatment are limited. This association study was designed to assess the difference in genome-wide methylation patterns between individuals with OUD in methadone maintenance treatment (MMT) ( = 114) and those with OUD who achieved long-term abstinence (>10 years) without mu opioid receptor agonist treatment ( = 136). - Source: PubMed
Publication date: 2026/05/05
Levran OrnaLi JustinSason AnatAdelson MiriamPeles Einat - Only recently have human postmortem brain studies of differential gene expression (DGE) associated with opioid overdose death (OOD) been published; sample sizes from these studies have been modest (N = 40-153). To increase statistical power to identify OOD-associated genes, we leveraged human prefrontal cortex RNA-seq data from four independent OOD studies and conducted a transcriptome-wide DGE meta-analysis (N = 272). Using a unified gene expression data processing and analysis framework across studies, we meta-analyzed 20, 098 genes and found 335 significant differentially expressed genes (DEGs) by OOD status (false discovery rate < 0.05). Of these, 66 DEGs were among the list of 303 genes reported as OOD-associated in prior prefrontal cortex molecular studies (e.g., genes/gene families OPRK1, NPAS4, DUSP, EGR). The remaining 269 DEGs were not previously reported (e.g., NR4A2, SYT1, HCRTR2, BDNF). There was little evidence of genetic drivers for the observed differences in gene expression between opioid addiction cases and controls. Enrichment analyses for the DEGs across molecular pathway and biological process databases highlight an interconnected set of genes and pathways linked to orexin and tyrosine kinase receptors through MEK/ERK/MAPK signaling to affect neuronal plasticity. - Source: PubMed
Publication date: 2026/05/08
Carter Javan KQuach Bryan CWillis CarynMinto Melyssa SHancock Dana BMontalvo-Ortiz JanitzaCorradin OliviaLogan Ryan WWalss-Bass ConsueloMaher Brion S Johnson Eric Otto