DCXR Human Protein
- Known as:
- DCXR Human Protein
- Catalog number:
- GWB-BSP155
- Product Quantity:
- 1000ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- DCXR Human Protein
Related genes to: DCXR Human Protein
- Gene:
- DCXR NIH gene
- Name:
- dicarbonyl and L-xylulose reductase
- Previous symbol:
- -
- Synonyms:
- KIDCR, DCR, SDR20C1
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-07-25
- Date modifiied:
- 2018-07-10
Related products to: DCXR Human Protein
Related articles to: DCXR Human Protein
- Gestational diabetes mellitus (GDM) poses significant health risks, yet the causal genetic and epigenetic mechanisms linking glycolipid metabolism dysregulation to GDM remain elusive. This study aimed to identify key causal genes and regulatory pathways by integrating multi-omics data with large-scale genetic association studies. - Source: PubMed
Publication date: 2026/05/20
Lin XiaoxiaoZheng JingjingQin NingningLi Yimei - Recent evidence has established a significant link between N4 acetylcytidine (ac4C) mRNA modification, mediated by N Acetyltransferase 10 (NAT10), and bone metabolism. Nonetheless, the precise role and regulatory targets of NAT10, along with its associated ac4C modification in human bone formation, remain inadequately characterized. This study employed bioinformatics analysis of transcriptomic datasets from primary osteoblasts of individuals with high versus low bone mineral density (BMD), alongside a curated set of ac4C-modified genes, to identify key differentially expressed genes (DEGs) regulated by this pathway within an osteogenic context. Overall, eleven key NAT10/ac4C-associated DEGs linked to BMD status were identified: CFD, CTSF, DCXR, FADS1, GOLIM4, IMPA2, MLEC, NCLN, NT5DC2, PTGFRN, and VASP. Notably, FADS1, NT5DC2, and PTGFRN emerged as crucial ac4C-modified genes across three machine learning models. Furthermore, the tri-gene signature (FADS1/NT5DC2/PTGFRN) showed excellent diagnostic performance in distinguishing different BMD statuses. In vitro validation using MC3T3-E1 osteoblastic cells revealed that the knockdown of NAT10 via lentiviral delivery markedly impaired cell proliferation and osteogenic differentiation. This impairment was evidenced by the results of the CCK-8 proliferation assay, alkaline phosphatase staining, and Alizarin Red staining. Additionally, qRT PCR analysis demonstrated a significant downregulation of FADS1 and NT5DC2 expression subsequent to NAT10 knockdown. These findings underscore the role of NAT10-mediated ac4C modification as a pivotal regulator of osteoblast activity and gene expression programs associated with BMD. This research offers novel insights into the regulation of bone metabolism and proposes potential diagnostic markers and therapeutic targets for osteoporosis. - Source: PubMed
Tang YWang QDong WJiang GLei MHu XWu YJiang WHao JHu Z - The World Health Organisation (WHO) recommends digital chest radiography (dCXR) with computer-aided detection (CAD) for tuberculosis (TB) screening of individuals >15 years of age. - Source: PubMed
Publication date: 2026/04/30
Nyangu SarahMulenga HumphreyMendelsohn Simon CPerumal TahliaTameris MicheleMoloantoa TumeloMalherbe Stephanus TNoor FirdowsShenje JustinTredoux NicoletteKany Luabeya Angelique KanyMaruri FernandaPanchia RavindreHlongwane KhuthadzoStanley Kimvan der Heijden Yuri FHadley KateMartinson NeilDheda KeertanLeslie AlFourie BernardWalzl GerhardScriba Thomas JSterling Timothy RHatherill Mark - The World Health Organization recommends community-based tuberculosis active case finding using digital chest radiography with computer-aided detection (dCXR/CAD) and/or molecular diagnostics, but clinical and economic outcomes are unclear. - Source: PubMed
Publication date: 2026/03/30
Deleger Julie NKhatami S NazaninJones MichelleJalali Mohammad SPaltiel A DavidWong Emily BFlorance GradyFreedberg Kenneth AWood RobinHorsburgh C RobertReddy Krishna P - Migraine and Meniere’s disease (MD) show high clinical comorbidity, shared symptoms such as vertigo and overlapping mechanisms like neurogenic inflammation suggest common pathophysiology. However, the core immunogenetic drivers underlying this comorbidity, particularly at cellular resolution, remain uncharacterized. - Source: PubMed
Publication date: 2026/04/18
Hu XiaoWang YangYu Si-JiePan Chun-YaLiang Bing-YuJiang Shang-ShangChen Shan-WenHan Yan-Xun