Anti-Mouse CD73 PE 100 ug
- Known as:
- Antibody toMouse CD73 PE 100 ug
- Catalog number:
- 12-0731-82
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD73 100
Related genes to: Anti-Mouse CD73 PE 100 ug
- 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: Anti-Mouse CD73 PE 100 ug
Related articles to: Anti-Mouse CD73 PE 100 ug
- Human dental pulp is a complex tissue composed of diverse cell types, including mesenchymal stromal cells (MSCs), which are crucial for tissue repair and regeneration. Although single-cell RNA sequencing (scRNA-seq) data from human dental pulp have accumulated in recent years, MSC identification relies on manual verification of marker genes after clustering, which limits analytical efficiency and scalability. The choice of clustering resolution is determined empirically, potentially leading to under- or over-segmentation of MSCs or their mixing with other cell types. The objective of this study was to establish a computational workflow that automatically extracted uncultured MSCs from human dental pulp scRNA-seq data and to investigate the characteristics of freshly-isolated MSCs in dental pulp using multiple public datasets. - Source: PubMed
Publication date: 2026/07/07
Okada DaigoTakeda-Kawaguchi TomokoTezuka Ken-Ichi - Cellular senescence, mediated by CDKN2A-encoded p16, generates a senescence-associated secretory phenotype (SASP) that may promote immune evasion in solid tumors. Recent immunohistochemical studies have identified associations between p16 over-expression and CD8+ T cell exclusion in gastric adenocarcinoma, but transcriptomic validation and mechanistic characterization remain limited. - Source: PubMed
Publication date: 2026/07/01
Lehrer StevenRheinstein Peter - Extracellular 5'-nucleotidase (NT5E/CD73) plays a pivotal role in the tumor immune microenvironment by catalysing the production of adenosine. This study aims to evaluate the expression and function of NT5E in colorectal cancer progression, and to explore its potential as a novel biomarker and for associated immunotherapy. - Source: PubMed
Publication date: 2026/06/30
Wu WeixingCheng ChengYang TaoMeng WeishanWang Yimin - While CD73 and CD155 are implicated in immune evasion and tumor progression, their roles in pleural mesothelioma (PM) remain unclear. Therefore, we investigated the association between CD73 and CD155 expression in resected epithelial PM specimens and explored their impact on 5-year progression-free survival (PFS) and 5-year overall survival (OS). - Source: PubMed
Nabe YusukeFujita YasuhiroHashimoto TeppeiTanaka KanjiManabe TakehikoYoshimatsu KatsumaNemoto YukikoNishizawa NatsumasaOyama RintaroHonda YoheiMori MasatakaMatsumiya HirokiKanayama MasatoshiTaira AkihiroTakenaka MasaruKuroda KojiShimajiri ShoheiTanaka Fumihiro - Background Metabolic disorders associated with elevated saturated fatty acids are linked to chronic inflammatory diseases, including periodontitis, yet the mechanisms connecting lipotoxic stress to gingival inflammation remain unclear. This study investigated how palmitate-induced metabolic stress affects purinergic signaling, mitochondrial function, and endoplasmic reticulum (ER) stress in murine gingival fibroblasts (mGF), and whether adenosine modulates these effects. Methods mGF were treated with BSA control, palmitate, IL-1β, or palmitate plus IL-1β, followed by bulk RNA sequencing, Seahorse metabolic analysis, biochemical assays, and transmission electron microscopy. Results Palmitate suppressed expression of key adenosine-generating ectoenzymes and purinergic signaling genes, including Cd73 (Nt5e), Cd39 (Entpd1), Adk, Ada, and adenosine receptors. Concurrently, palmitate amplified IL-1β-induced inflammatory mediators such as Cxcl1, Cxcl2, Cxcl5, Ccl2, and Il6. Gene ontology analysis demonstrated enrichment of pathways related to innate immune activation, oxidative stress, mitochondrial dysfunction, ER stress, and purine metabolism. Palmitate also induced intracellular lipid accumulation and mitochondrial dysfunction, evidenced by reduced NAD+/NADH ratio, increased mitochondrial reactive oxygen species (ROS), elevated protein oxidation, and increased proton leak despite enhanced electron transport chain protein expression. Ultrastructural analyses revealed swollen mitochondria, ER expansion, and increased ER-mitochondrial associations. Mechanistically, palmitate activated the Perk-eIF2α-Atf4 ER stress pathway, increasing phosphorylation of Perk and eIF2α and elevating Atf4 expression. Extracellular adenosine attenuated mitochondrial ROS accumulation, reversed Perk and Atf4 activation, improved mitochondrial respiration, and preserved ER and mitochondrial ultrastructure. Conclusions Palmitate disrupts the Cd73-adenosine axis while promoting mitochondrial dysfunction, oxidative stress, and Perk-mediated ER stress in gingival fibroblasts. Adenosine signaling protects against lipotoxic-induced ER stress, highlighting the Cd73-adenosine pathway as a potential therapeutic target in metabolically driven periodontal inflammation. - Source: PubMed
Publication date: 2026/06/15
Dawson ShantieceBatan SoniaAdams NinaBombin SergeiRamos-Junior Erivan SMorandini Ana Carolina