Ask about this productRelated genes to: MOCOS antibody
- Gene:
- MOCOS NIH gene
- Name:
- molybdenum cofactor sulfurase
- Previous symbol:
- -
- Synonyms:
- HMCS, FLJ20733, MOS
- Chromosome:
- 18q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-18
- Date modifiied:
- 2016-10-05
Related products to: MOCOS antibody
Related articles to: MOCOS antibody
- Central compartment atopic disease (CCAD) is an early stage of type 2 chronic rhinosinusitis (CRS), characterized by type 2 inflammation and frequent olfactory dysfunction, primarily due to olfactory cleft (OC) obstruction. - Source: PubMed
Publication date: 2026/04/29
Pan XingchenLi YankunJiang XincenBleier Benjamin SXie LifengZhang YinghongWu Dawei - 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 - The impact of metabolism-related genes on inflammatory bowel disease remains unclear. This study aimed to identify the causal relationships between metabolism-related genes and inflammatory bowel disease. - Source: PubMed
Publication date: 2026/01/22
Zhou HanXie KexinAn HongjinFeng YueYuan YifanGan Huatian - Clear cell renal cell carcinoma (ccRCC) is characterized by marked intratumor heterogeneity (ITH), which contributes to therapeutic resistance and poor clinical outcomes. We aimed to develop a robust prognostic model for stratifying patients with ccRCC on the basis of ITH. - Source: PubMed
Publication date: 2025/12/10
Filho Valbert Oliveira CostaPassos Pedro Robson CostaNoronha Mariana MacambiraSaldanha Erick FChangsu Park LawrenceLopes Carlos Diego HolandaLeite Giuseppe G F - Xanthinuria type II is a rare hereditary disorder caused by mutations in the MOCOS gene, leading to dual deficiency of xanthine dehydrogenase and aldehyde oxidase. To establish a robust animal model for this condition, we generated Mocos knock-in (KI) rats carrying the Arg419Ter nonsense mutation identified in Japanese patients. Homozygous KI rats exhibited severe growth retardation, anemia, and reduced survival, with all individuals dying by 14 weeks of age. Biochemical analyses revealed elevated levels of hypoxanthine and xanthine, along with decreased uric acid in both serum and urine, confirming xanthinuria. Homozygous KI rats also showed increased blood creatinine (CRE) and urea nitrogen (UN), and decreased urinary CRE and UN, indicating renal dysfunction. Histopathological examination showed obstructive nephropathy characterized by tubular atrophy, crystal deposition, and inflammation. Compared to existing mouse models, Mocos KI rats demonstrated extended lifespan, enabling more detailed investigation of disease mechanisms. This rat model provides a valuable tool for studying the pathogenesis of xanthinuria type II and exploring potential therapeutic strategies. - Source: PubMed
Publication date: 2025/12/03
Urasaki MaoNagasaka KanaKido MinoriHayashi KentaWatanabe AyumiHattori KosukeSekiguchi TakahiroKuwamura MitsuruTanaka MiyuuMashimo TomojiKuramoto Takashi