Mouse Anti-Human CD73
- Known as:
- Mouse Antibody toHuman CD73
- Catalog number:
- 129-10168
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human CD73
Related genes to: Mouse Anti-Human CD73
- Gene:
- NT5E NIH gene
- Name:
- 5'-nucleotidase ecto
- Previous symbol:
- NT5
- Synonyms:
- CD73, eN, eNT, CALJA
- Chromosome:
- 6q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-02-23
- Date modifiied:
- 2016-10-05
Related products to: Mouse Anti-Human CD73
Related articles to: Mouse Anti-Human CD73
- The classical adenosinergic pathway (CD39/CD73/A2BR) plays a pivotal role in regulating tumor immune evasion in hepatocellular carcinoma (HCC). However, the prognostic significance of the specific spatial coordination of these enzymes within the tumor microenvironment remains elusive. - Source: PubMed
Publication date: 2026/09/30
Liu YaoWang BinghanGuo YuanFan ChenZhao WeiLu LigongChen GuodongLiu WeifengZhan Meixiao - Dental pulp stem cells (DPSCs), a subset of mesenchymal stem/progenitor cells, exhibit remarkable self-renewal and multipotent differentiation capacity, making them promising candidates for regenerative applications. While their in vitro characteristics have been extensively studied, the in vivo dynamics and molecular regulation during development are much less known. This study examined the embryonic/prenatal (E16.5) and early postnatal (P3.5 and P7.5) stages of mouse molar development to trace the temporospatial expression and overlap of five key molecules associated with DPSC: a trio of positive markers (CD73/Nt5e, CD90/Thy1, and CD105/Eng) and two negative markers (CD34/Cd34 and CD45/Ptprc). Reanalysis of single-cell RNA sequencing data revealed a triple-positive and double-negative population overlapping in the dental mesenchyme by P7.5. The results were confirmed by multiple immunofluorescence-based in situ labeling. These findings contribute to the understanding of the spatiotemporal in vivo expression landscape and dynamics of DPSC markers, thus bridging the gap between in vitro characterization and the complex developmental reality of the dental pulp. - Source: PubMed
Publication date: 2026/09/24
Holomková KateřinaYamada ShuntaroŠvandová EvaMatalová EvaHovhannisyan Jesica HasmikKrikorian TaleenBagdasarian LidiiaAyvazyan SonaAzadians DinoLesot HervéJanečková Eva - Goose astrovirus-2 (GAstV-2) is the major etiological agent responsible for hyperuricemia and visceral gout in goslings, which causes substantial economic losses to the goose-raising industry. However, the complete pathogenic mechanisms underlying GAstV-2-induced hyperuricemia have not been fully elucidated. In this study, 1-day-old healthy Yangzhou goslings were orally inoculated with GAstV-2 to establish a viral infection model. The effects of GAstV-2 infection on growth performance, serum uric acid levels, cecal microbiota structure, and renal gene expression of goslings were systematically investigated. The results showed that GAstV-2 infection caused a cumulative mortality rate of 10%-30% in goslings and significantly impaired growth performance, as reflected by decreased average daily gain and average daily feed intake as well as an increased feed-to-gain ratio (P < 0.05). In addition, GAstV-2 challenge induced severe histopathological damage to the liver and kidney, disordered serum biochemical metabolism, and excessive release of pro-inflammatory cytokines, accompanied by a significant elevation in serum uric acid levels (P < 0.05). The 16S rRNA high‑throughput sequencing results confirmed that GAstV‑2 infection significantly decreased the abundances of uric acid‑degrading beneficial bacteria, including Paenibacillus polymyxa, Oscillospira guilliermondii, and Lactococcus lactis, while markedly increasing the abundance of Clostridium perfringens, which is closely associated with uric acid synthesis. Renal transcriptomic analysis confirmed that key genes involved in purine metabolism, including PRPS, IMPDH1, and NT5E, were significantly upregulated in the kidney tissues of infected goslings, which was closely correlated with the occurrence of hyperuricemia. In conclusion, GAstV-2 infection markedly inhibits growth, triggers hepatic and renal injury, increases serum uric acid and inflammatory levels, and remodels the intestinal microbiota composition and renal transcriptomic profiles in goslings. This study systematically explored the influences of GAstV-2 infection on growth performance, hepatorenal injury, and serum uric acid metabolism in goslings, and preliminarily revealed the potential underlying mechanism of GAstV-2-induced hyperuricemia by separately analyzing intestinal microbiome and renal transcriptome data. These findings provide fundamental data and a theoretical basis for further elucidating the pathogenic mechanism of GAstV-2 and developing targeted prevention and control strategies against gosling gout. - Source: PubMed
Publication date: 2026/09/22
Fan JunyangMao SaiYan BingxueWang MengxiangZhang JingZhang Hongying - Extracellular purinergic signaling, mediated by nucleotides such as adenosine triphosphate (ATP) and adenosine, is a critical regulator of retinal homeostasis. Within the retina, this signaling pathway is indispensable for maintaining physiological functions. Dysregulation of extracellular purine balance is a key driver of retinal pathophysiology, contributing to inflammation, pathological angiogenesis, and neurodegeneration in diseases like diabetic retinopathy (DR), age-related macular degeneration (AMD), glaucoma, and retinopathy of prematurity (ROP). The hydrolysis of extracellular ATP to adenosine, primarily orchestrated by the sequential actions of NTPDase1/ENTPD1 (CD39) and ecto-5'-nucleotidase/NT5E (CD73), represents a fundamental mechanism for calibrating purinergic signals and shifting the microenvironment from pro-inflammatory to anti-inflammatory and protective. CD39 and CD73 are pivotal enzymes in regulating retinal purinergic equilibrium. Despite their well-characterized roles in tumor biology and cerebral pathophysiology, the expression, physiological functions, and pathological implications of CD39/CD73 in the retina remain understudied and lack systematic synthesis. This review synthesizes current understanding of the roles of CD39 and CD73 in retinal physiology and pathology, with a focus on their implications in DR, AMD, glaucoma, and ROP. Critically, this review provides the first systematic integration of their layer-specific spatial compartmentalization, context-dependent functional duality, and emerging metabolic roles in photoreceptor homeostasis. We also discuss emerging therapeutic strategies that target this pathway, addressing the growing need for translational research to preserve vision. - Source: PubMed
Publication date: 2026/09/08
Chen XinyiJi JingYao JiaxinChen PengfanZhang JialiLiu LongqianWen Xiangyi - Diabetic kidney disease (DKD) is commonly staged using albumin-to-creatinine ratio (ACR) and estimated glomerular filtration rate (eGFR), yet complementary molecular markers are needed. We profiled urine and serum metabolites from 92 Korean participants (72 with type 2 diabetes and 20 healthy controls) using gas chromatography-tandem mass spectrometry (GC-MS/MS) and liquid chromatography-tandem mass spectrometry (LC-MS/MS). An exploratory restricted Boltzmann machine framework compared five DKD staging criteria and prioritized candidate metabolites; robustness was assessed against LASSO, linear support vector machine (SVM), and random forest using nested cross-validation. ACR-based staging showed the highest metabolomic discrimination. Urinary adenosine and 5'-methylthioadenosine decreased, whereas serum N2,N2-dimethylguanosine and -aconitic acid increased across ACR stages. Integration with a public renal tubular microarray dataset suggested as a cross-study network hub. These cross-sectional findings define candidate metabolite signatures associated with DKD severity and require external longitudinal validation before clinical translation. - Source: PubMed
Publication date: 2026/09/12
Jung InhaPark SungjinJi MoongiPark So YoungLee Da YoungYu Ji HeeSeo Ji APaik Man-JeongPark Hyeong KyuKwon Soon HyoLee Dae HoKim Nan Hee