Ask about this productRelated genes to: RORA antibody
- Gene:
- RORA NIH gene
- Name:
- RAR related orphan receptor A
- Previous symbol:
- -
- Synonyms:
- RZRA, ROR1, ROR2, ROR3, NR1F1
- Chromosome:
- 15q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-04-13
- Date modifiied:
- 2016-10-05
Related products to: RORA antibody
Related articles to: RORA antibody
- Sepsis-induced immunosuppression is a key factor contributing to high mortality rates. However, suitable biomarkers for routine clinical monitoring of immune function are currently lacking. Serum cholinesterase levels are markedly diminished in sepsis and are associated with unfavorable prognoses, its role in the immunosuppression pathology and the mechanisms involved remain inadequately understood. - Source: PubMed
Publication date: 2026/05/07
He QianHuang Xu - Hypothalamic arginine vasopressin (AVP) and oxytocin (OXT) magnocellular neurons (MCNs), share a developmental lineage. The transcription factors driving specification are yet unknown. Using gene regulatory network analysis on published single-cell RNA-sequencing data of the developing mouse hypothalamus, we identified RORA, EBF3, FOXP1, FOXP2, and BCL11B as candidate transcription factors for differential MCN specification. We modeled developmental gene expression dynamics using computational cell fate mapping, revealing enrichment of EBF3 and BCL11B in the lineage, and FOXP1 and FOXP2 in the lineage. analysis of and promoters predicted a binding site for FOXP1 and FOXP2, and assay identified regulation on both and genomic promoters. Finally, heterozygous FOXP1 knockout mice exhibited a significant reduction in AVP and OXT neuron abundance, with OXT neurons disproportionally affected. We conclude that FOXP1 participates in MCN development, while being differentially active in OXT MCNs relative to AVP MCNs. - Source: PubMed
Publication date: 2026/04/04
Berkhout Jari BTrender SophieKrabichler QuirinPodpecan YuvalFranke FelixSchubert TimBurbach PeterGrinevich ValeryAdan RogerFröhlich HenningAlthammer FerdinandMeijer Onno CMahfouz Ahmed - The mammalian pineal gland maintains normal circadian rhythms and homeostasis by secreting melatonin. However, the lack of a single-cell-resolved regulatory map limits our understanding of how these neuroendocrine functions are orchestrated. Here, we constructed a multiomics atlas of the pineal gland from by integrating snRNA-seq, snATAC-seq, and spatial transcriptomics. We identified pinealocytes as the predominant cell type, alongside six glial and vascular lineages. Chromatin accessibility analysis delineated cell-type-specific regions enriched for melatonin synthesis and phototransduction genes. Notably, we resolved a dual-layer regulatory architecture: While melatonin synthesis programs are robustly organized, circadian clock regulators exhibit a distinct, sparse spatial pattern. Coexpression networks further identified core modules and regulatory hubs-including CRX/OTX2, LHX4, and RORA-that integrate these circadian and light-responsive signals. Cell-cell communication analysis identified signaling axes, such as -/, -, and -, that potentially coordinate this spatial functional organization. Integrating genetic traits showed that sleep and neuropsychiatric risk variants preferentially map to these pineal regulatory modules. Specifically, sleep-associated loci converged on -linked elements, while bipolar disorder-associated loci highlighted candidate genes of and . Overall, this study reveals the cellular diversity and spatial regulatory logic of the primate pineal gland, providing a physiological foundation for investigating circadian and neuroendocrine regulation in healthy and disease models. - Source: PubMed
Publication date: 2026/05/05
Zheng JihongXiao YuchenLyu JianjunXu HongtaoZhang YaqunLi YanchuanLi YihaoWang TianjunLiu LiuJin LingjingZhou XuhuiZhang Chao - The transition from acute inflammation to chronic pain represents a significant clinical challenge, often driven by a failure of endogenous resolution programs. Specialized pro-resolving mediators (SPMs), derived from polyunsaturated fatty acids, are crucial for actively terminating inflammation and restoring tissue homeostasis. Maresin 1 (MaR1), a prototypical SPM biosynthesized from docosahexaenoic acid (DHA), has emerged as a powerful modulator of pain. This review comprehensively synthesizes the current preclinical evidence, primarily derived from preclinical animal models, detailing the analgesic effects of MaR1 across a spectrum of pain models, including inflammatory, neuropathic, postoperative, osteoarthritis-related pain, etc. We dissect the multifaceted mechanisms underlying its efficacy, which extend beyond simple anti-inflammation. MaR1 exerts its effects by: (1) attenuating neuroinflammation including the suppression of glial (microglia and astrocyte) activation and reprogramming macrophage phenotypes; (2) directly modulating neuronal function by inhibiting nociceptive ion channels (e.g. TRPV1) and reversing central synaptic plasticity; and (3) promoting robust tissue repair, including peripheral nerve regeneration. These actions are mediated through potential specific receptors, notably G-protein-coupled receptor 37-like 1 (GPR37L1) on glial cells and retinoic acid-related orphan receptor α (RORA) on neurons. While MaR1 demonstrates significant therapeutic potential, challenges related to its pharmacokinetic instability and observed sex-dependent analgesic effects must be addressed for successful clinical translation. This review provides a comprehensive mechanistic framework supporting MaR1 as a next-generation therapeutic candidate for pain management, and outlines the core research directions to overcome key translational barriers for MaR1-based therapies. - Source: PubMed
Publication date: 2026/04/25
Wang FuquanYang YangWang WenShi QingFan Bifa - Autism Spectrum Disorder (ASD) is a genetically heterogeneous neurodevelopmental condition involving multiple genes. This study aimed to comprehensively review the genetic landscape of ASD in the Iranian population, identifying gene variants associated with increased risk, to facilitate improved diagnosis and targeted interventions. A systematic review and meta-analysis were conducted on genetic association studies of ASD in Iran up to August 2025. Comprehensive searches were performed in PubMed, Scopus, Web of Science, and Persian databases using relevant keywords. Quality assessment was performed using the Joanna Briggs Institute critical appraisal tools. Meta-analyses were carried out using Review Manager software, assessing heterogeneity and publication bias. Protein-protein interaction networks were constructed via STRING and analyzed with Cytoscape to identify key hub genes and enriched neurodevelopmental pathways. In this study, genes RORA, MTRR, MTR, Reelin, VDR, VMAT1, ACE I/D, MOCOS, HOTAIR, ANRIL, RIT2, MMP-9, GRM7, FOXP3, and GRIN2B showed significant associations with the occurrence of autism. Findings reinforce associations between multiple gene polymorphisms, especially RORA rs4774388 and MOCOS rs594445, with the risk of ASD. This systematic review and meta-analysis emphasize the multifactorial genetic contributions to ASD in the Iranian population, highlighting key risk loci and neurodevelopmental pathways. The findings underscore the importance of integrating genetic, epigenetic, and environmental factors for understanding ASD etiology and developing population-tailored diagnostic and therapeutic strategies. Future studies employing larger cohorts and multi-omics approaches are warranted to further elucidate the complex genetic architecture of ASD in diverse ethnic groups. - Source: PubMed
Barfeh DelaramShahesmaeilinejad ArmitaEslami Shahrbabaki MahinKaramooz AnahitaShekari FatemehZare Arashlouei Azam