Mouse Anti Human CD73 CD73
- Known as:
- Mouse Anti Human CD73 CD73
- Catalog number:
- ant-414
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- Mouse Anti Human CD73
Related genes to: Mouse Anti Human CD73 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 CD73
Related articles to: Mouse Anti Human CD73 CD73
- Cervical cancer (CC) is the fourth most prevalent malignancy among women. The present study employed bioinformatics analyses to identify tumor mechanics-related genes (TMRGs), establish a prognostic model, and investigate the association of tumor stiffness with pivotal genes utilizing clinical samples. - Source: PubMed
Publication date: 2026/06/03
Zhang LuFu HaonanFeng YaliTian JianxinGao XueShang Yuhong - Glioblastoma (GBM) represents an immunologically "cold" and metabolically suppressive tumor characterized by profound T-cell exhaustion, hypoxia-induced adenosinergic signaling, and resistance to checkpoint blockade. Converging evidence identifies lymphocyte-activation gene 3 (LAG-3) and the CD39/CD73 ectonucleotidase cascade as cooperative regulators of immune dysfunction within the GBM microenvironment. LAG-3 attenuates TCR/CD3 signaling and disrupts mitochondrial oxidative phosphorylation, diminishing effector T-cell persistence. Concurrently, CD39/CD73-mediated ATP hydrolysis elevates adenosine levels, activating A₂A receptors that inhibit glycolysis, suppress IFN-γ, and promote Treg and M2 macrophage polarization. Spatial and single-cell omics reveal co-localization of LAG-3⁺ exhausted T cells with CD73⁺ stromal and myeloid niches, suggesting a reciprocal immunometabolic feedback loop reinforcing exhaustion. This review elucidates the molecular crosstalk between LAG-3 signaling and the adenosine pathway, emphasizing key metabolic regulators including AMPK, mTOR, and HIF-1α. It further evaluates therapeutic strategies combining LAG-3 or PD-1 blockade with adenosine receptor antagonists or CD73 inhibitors to restore T-cell bioenergetics and antitumor activity. By integrating mechanistic immunometabolism with translational insights, this review establishes a dual-pathway framework of checkpoint synergy underlying resistance in GBM and proposes rational combination immunotherapies to reverse metabolic and immune exhaustion. - Source: PubMed
Publication date: 2026/06/15
Mukherjee Arpita - Intrahepatic cholangiocarcinoma (ICC) is an aggressive liver malignancy with a rising global incidence and limited therapeutic options. Vascular invasion (VI) is a hallmark of advanced disease, correlating with early recurrence and dismal prognosis, yet its tumor microenvironment (TME) drivers remain elusive. We analyzed single-cell RNA sequencing (scRNA-seq) data from 25 ICC samples to systematically characterize the cellular composition and molecular features related to VI. By integrating bulk RNA-seq data, spatial transcriptomics, and multiplex immunofluorescence, we identified a distinct subset of tumor-like cancer-associated fibroblasts (CAFs), termed tCAFs, enriched in VI-positive tumors. Functional enrichment analyses revealed that tCAFs were prominently associated with hypoxia and angiogenesis pathways, findings corroborated by the significant upregulation of tCAF markers ( and ) in ICC-derived CAFs under hypoxic conditions in vitro. Cell-cell communication analysis and spatial mapping uncovered that tCAFs might promote VI primarily through VEGF signaling interactions with endothelial cells. Integrative bioinformatics and RT-qPCR validation identified three key functional genes in tCAFs: , , and . In endothelial sprouting assays, pharmacological inhibition of exerted a pronounced suppressive effect. Consistently, sprouting assays using ICC-derived CAFs with knockdown confirmed that its downregulation significantly reduced endothelial sprouting capacity. Importantly, administration of the inhibitor BAY-876 effectively suppressed tumor progression and intrahepatic metastasis in the orthotopic ICC mouse model. Our findings define a VI-associated cellular ecosystem and molecular landscape in ICC, unveiling a novel hypoxia-tCAFs-endothelial cells axis. Furthermore, we identify as a clinically relevant therapeutic target, offering new insights into tumor VI. - Source: PubMed
Publication date: 2026/05/31
Fan JianingTong MengLu YunkunWang QianqianXie YangyangLin KainanXu JunjieCai XiujunLiang Xiao - Small extracellular vesicles (sEVs) derived from mesenchymal stem/stromal cells (MSCs) contain microRNAs (miRNAs) that can modulate the cellular behavior of recipient cells. Human periodontal ligament mesenchymal stem/stromal cells (hPDL-MSCs) are a unique MSC population involved in periodontal tissue regeneration; however, the specific miRNAs that regulate their proliferative and differentiation-related properties remain incompletely understood. In this study, we profiled miRNAs enriched in sEVs secreted by highly proliferative human PDL-MSCs and identified hsa-let-7c-3p as a candidate regulator of hPDL-MSC behavior. Functional assays demonstrated that hsa-let-7c-3p enhanced proliferative and migratory behavior, reflected by an approximately 1.5-fold increase in metabolic activity and a 2-fold increase in migration, while suppressing osteogenic differentiation, with approximately 50% reductions in alkaline phosphatase activity and mineralization. To identify functionally relevant downstream targets, we intersected AGO2-RIP-seq-enriched transcripts, RNA-seq-defined genes altered by hsa-let-7c-3p overexpression, and in silico target predictions, identifying NT5E/CD73 as a candidate downstream target with experimental validation. Furthermore, NT5E knockdown partially phenocopied the effects of hsa-let-7c-3p overexpression on hPDL-MSC proliferation, migration, and osteogenic differentiation, supporting a functional link between hsa-let-7c-3p and NT5E/CD73. These findings highlight hsa-let-7c-3p as an underexplored sEV-associated 3p miRNA strand that restrains the proliferation-to-osteogenesis transition of hPDL-MSCs and identify NT5E/CD73 as a functionally relevant downstream target. Clinical trial number. Not applicable. - Source: PubMed
Publication date: 2026/06/02
Myint Ye Yint KaungLiu AnhaoGao JingyiHatasa MasahiroSrithanyarat Supreda SuphanantachatIwata Takanori - Adenosine, generated by CD73/NT5E, is a critical endogenous regulator of immune-mediated inflammation. Genetic variants in have been linked to vascular and inflammatory phenotypes. Systemic lupus erythematosus (SLE) is a chronic autoimmune disease marked by persistent inflammation. Using a systems biology approach, we examined immunologic and genetic alterations in adenosine signaling in SLE. Whereas gene signatures associated with extracellular adenosine production were elevated in lupus-affected tissues, adenosine-mediated immunosuppressive pathways were broadly downregulated and correlated with increased proinflammatory signatures. Analysis of the single-nucleotide polymorphism rs2229524, which introduces a non-synonymous amino acid change, predicted impaired enzymatic function and was associated with reduced adenosine immunomodulation and increased rates of pericarditis and hypertension in SLE patients. These findings highlight the importance of extracellular adenosine signaling in regulating immune-mediated inflammation in SLE and highlight the role of a loss-of-function variant in contributing to tissue injury. - Source: PubMed
Publication date: 2026/05/21
Peabody IsaacOlferiev MikhailOwen Katherine ADawson TysonBachali PrathyushaKasson PeterGrammer Amrie CCrow Mary KLipsky Peter E