Monkey CD70 antigen(CD70) ELISA kit
- Known as:
- Monkey CD70 antigenic(CD70) Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- e09c1493
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Blue gene shanghai
- Gene target:
- Monkey CD70 antigen(CD70) ELISA kit
Related genes to: Monkey CD70 antigen(CD70) ELISA kit
- Gene:
- CD70 NIH gene
- Name:
- CD70 molecule
- Previous symbol:
- CD27LG, TNFSF7
- Synonyms:
- CD27L
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-08
- Date modifiied:
- 2016-10-05
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- Weight loss remains one of the primary strategies for reducing cardiometabolic risk, particularly with the advent of glucagon-like peptide-1 receptor agonists, which have been demonstrated to induce significant weight loss. Recent evidence suggests, however, that weight loss does not completely normalize the underlying biology of obesity. When weight loss medications are discontinued, patients may regain lost weight along with an increase in cardiometabolic disease risk, indicating that these medications may contribute to transiently altering the phenotype of obesity, but do not produce long-term remission. Adipose tissue is increasingly recognized as an active organ regulating systemic inflammation and metabolic homeostasis. In obesity, adipose tissue becomes inflamed through the activation of innate and adaptive immune pathways. This response has a lasting effect on the immune system. T cells in adipose tissue develop memory-like qualities via epigenetic and transcriptional reprogramming and can persist after weight loss, ready for rapid activation upon renewed metabolic stress. These immunologic memory effects drive repeated weight gain, progressive metabolic dysfunction, and ongoing cardiovascular risk. An immune process is working alongside the endocrine and metabolic adjustments that facilitate energy conservation and fat regain. The repetitive cycles of weight loss and regain further amplify these responses, leading to greater inflammation. Memory T-cell populations are maintained primarily through the CD70-CD27 axis; therefore, targeting this axis may be an effective approach to developing therapies that modify immune memory and achieve long-term cardiometabolic remission when combined with weight loss. - Source: PubMed
Publication date: 2026/06/15
Sami NabeelParikh Manish AMihatov NinoSchwartzman Michal LaniadoFrishman William HPeterson Stephen J - Chronic ultraviolet (UV) exposure drives the development of non-melanoma skin cancers (NMSCs), particularly cutaneous squamous cell carcinoma (cSCC), through persistent DNA damage and inflammation. However, how UV-induced epithelial damage is coupled to inflammatory signaling and tumor-stromal communication during skin carcinogenesis remains incompletely understood. Here, we identify CD70, a TNF superfamily member, as a UV- and DNA damage-inducible regulator that links epithelial stress responses to stromal activation and tumor-promoting signaling. Integrative analyses of transcriptomic (GTEx, GSE2503, GSE42677), proteomic (RPPA), and immunostaining datasets reveal robust upregulation of CD70 in sun-exposed skin, actinic keratoses, and cSCC lesions. Functionally, CD70 silencing suppresses cSCC proliferation and xenograft growth, whereas solar UV or DMBA exposure induces CD70 expression. CD70 depletion disrupts cytokine-receptor signaling and MAPK/NF-κB pathways and alters inflammatory gene expression in UV-irradiated keratinocytes. In dermal fibroblasts, CD70 enhances NF-κB activation and secretion of IL-6 and MCP3 in TGF-β-activated fibroblasts, thereby reinforcing paracrine inflammatory loops that support cSCC spheroid expansion and tumor progression. CD70 knockdown in fibroblasts abrogates these effects and reduces tumor proliferation and cytokine expression in vivo. Mechanistically, E2F1 directly binds and activates the CD70 promoter, linking the DNA damage response to CD70 upregulation. Collectively, our findings identify CD70 as a stress-inducible signaling hub that links DNA damage, inflammation, and tumor-stromal communication in skin carcinogenesis. Targeting CD70 may disrupt this feed-forward inflammatory circuit and provide a therapeutic strategy for UV-driven and inflammation-associated cSCC. - Source: PubMed
Publication date: 2026/06/11
Wang QiushiKhan Asad UHu ChengchengPetricoin Emanuel FMorris RebeccaDickinson Sally EWondrak Georg TLiu LiangBode Ann MGoldfarb Noah ICuriel-Lewandrowski ClaraZhang Tianshun - CD70, overexpressed in multiple myeloma (MM), is a promising target for theranostics. This study developed a CD70-targeted theranostic pair: the immuno-positron emission tomography tracer [Zr]Zr-DFO-ABDB6 and the therapeutic agent [Lu]Lu-DOTA-ABDB6, aiming to combine imaging and radiotherapy for MM. - Source: PubMed
Publication date: 2026/06/08
Li JunYan HaoyiWang XiaoyanZhang YouChen PingFeng JiaZhang RuiLi ZhanHuang ZixuanXu ChuanmianMa NingLin XiaohuaZhao MinyiZhu WenjingPeng QiyuXie SiweiWei WeijunDong Mengjie - T-cell activation requires firm arrest on APCs, a process essential for effective clonal expansion and differentiation. Although the role of co-inhibitory signals and integrin-mediated adhesion in modulating T-cell arrest is established, the contribution of co-stimulatory molecules to this process remains poorly understood. Here, we developed a quantitative "scan and stop" assay using engineered CHO cells as minimalistic APCs to systematically assess the influence of co-stimulatory proteins on T-cell arrest. These APCs express only selected peptide-MHC complexes and co-stimulatory ligands, allowing controlled investigation of their roles in both naïve and experienced CD4 and CD8 T cells. We found that CD40 selectively promotes the arrest of pre-activated CD4 T cells, whereas CD70 enhances the arrest of CD8 T cells, correlating with expression patterns of their respective receptors, CD40L and CD27. High-resolution imaging further revealed mechanical deformation of APCs during synapse formation, suggesting force generation by T cells. Altogether, our results identify CD40 and CD70 as subtype-specific regulators of T-cell arrest and reveal a novel dimension in co-stimulatory control of immune synapse formation. - Source: PubMed
Publication date: 2026/06/04
Gloe VincentSchregle RichardRatswohl ChristophRossy Jérémie - Objective To investigate the heterogeneity characteristics of cancer-associated fibroblasts (CAF) in acral melanoma (AM) and their functional roles in the tumor microenvironment (TME), providing a theoretical basis for developing effective therapeutic strategies. Methods The single-cell RNA sequencing data used in this study were previously generated by our research group and have been deposited in the HRA001804 dataset of the National Genomics Data Center (NGDC). Five AM patient samples were selected from this dataset for analysis, including 4 primary tumor samples (PL1, PL2, PL4, PL5) and 1 lymph node metastasis sample (LG2). Bioinformatics methods including unsupervised clustering, pseudotime trajectory analysis, transcription factor regulatory network analysis, and cell-cell communication analysis were used for data mining. Results Three subtypes of CAF were identified from 41 960 high-quality cells: immunomodulatory CAF (iCAF), myofibroblastic CAF (mCAF), and proliferative CAF (pCAF). Pseudotime trajectory analysis demonstrated that mCAF were located at the initiation of differentiation, while iCAF and pCAF were distributed in distinct terminal branches. FOS-like 1, AP-1 transcription factor subunit (FOSL1) was identified as a key transcription factor regulating the differentiation of CAF into pCAF, and its co-expression modules were enriched in the P53 signal pathway, AP-1 transcription factor network, and MYC-mediated cell proliferation pathways. Cell communication analysis revealed an interaction network centered on iCAF, with critical pathways including CSPG4-(ITGA2+ITGB1), GDF15-TGFBR2, LGALS9-CD45/CD44, and CD70-CD27 signal pathways. Conclusion CAF in AM exhibits high heterogeneity, with FOSL1 playing a key regulatory role in CAF differentiation. CAF participates in tumor microenvironment regulation through complex intercellular communication networks. These findings provide important insights into understanding the biological characteristics of acral melanoma and developing targeted therapeutic strategies. - Source: PubMed
Du ZhiminRao WeiWang YilinFeng JingyiZhao Hua