Anti_Human, mab CD229 Source Mouse
- Known as:
- Anti_Human, mab CD229 Source Mouse
- Catalog number:
- 101-M296
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Human mab CD229 Source Mouse
Related genes to: Anti_Human, mab CD229 Source Mouse
- Gene:
- LY9 NIH gene
- Name:
- lymphocyte antigen 9
- Previous symbol:
- -
- Synonyms:
- CD229, mLY9, SLAMF3, hly9
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-05
- Date modifiied:
- 2014-11-18
Related products to: Anti_Human, mab CD229 Source Mouse
Related articles to: Anti_Human, mab CD229 Source Mouse
- Type 1 diabetes (T1D) is a genetic autoimmune disease in children and young adults, with no cure, emphasizing the need for novel genetic-based therapies. Differential analysis using the "Limma" package identified 42 upregulated genes in the peripheral blood of T1D patients. Gene Ontology/Kyoto Encyclopedia of Genes and Genomes analysis suggested that CD38 may contribute to T1D development. LASSO (least absolute shrinkage and selection operator) machine learning successfully screened EMOES, SH2D1B, and TRDV3 from these upregulated genes. We selected SH2D1B, which is included in our natural killer cell-mediated cytotoxicity-related genes gene set, for further protein interaction network analysis, the analysis results revealed a highly correlated network of LY9, SH2D1B, CD244, and SLAMF6. Through immune infiltration analysis, we demonstrated resting natural killer (NK) cells and monocyte migration were upregulated, both were significantly related to the expression levels of LY9, SH2D1B, and CD244. Single-cell RNA sequencing analysis showed that both SH2D1B and CD244 were enriched in NK cells, and SH2D1B has the potential to modulate the function of NK cells. Subsequently, We performed gene set enrichment analysis with SH2D1B grouped into SH2D1Bhigh NK cells, SH2D1Blow NK cells, and SH2D1B- NK cells, which showed that the gene set related to the response to IFNγ is enriched in SH2D1Bhigh NK cells. With the analysis results, we performed differential expression analysis and validated the results by Western blotting. Finally, we identified activation of the IFNγ/JAK1/STAT/CD38 pathway in SH2D1Bhigh NK cells. Our findings suggest that SH2D1Bhigh NK cells may produce adenosine by IFNγ/JAK1/STAT/CD38, to limit autoimmunity and presumably disease development. - Source: PubMed
Chen JiahuiFu LinghuaGong YipengLiao LeYu WanqianYu PengXu GaosiYang Pingping - Hepatocellular carcinoma (HCC) is a highly prevalent and fatal digestive system malignancy, challenging to treat due to its latent onset and non-specific symptoms in advanced stages. Somatic mutations play a crucial role in hepatocarcinogenesis, with nearly half of HCC patients carrying oncogenic driver mutations such as TP53, CTNNB1, or TERT. In parallel, germline susceptibility variants identified by genome-wide association studies (GWAS) - including loci near TERT, MBOAT7, TM6SF2, and PNPLA3 - reveal inherited predisposition that shapes the molecular landscape for HCC development. Despite recent therapeutic advancements, long-term survival remains suboptimal, necessitating a deeper understanding of its pathogenesis and the identification of precise molecular targets. Traditional genomic studies, such as genome-wide association studies (GWAS), have successfully identified associated variants; however, due to their statistical design, they do not provide direct causal inference, functional supportive analyses, or comprehensive insight into multi-level molecular regulation and tumor microenvironment heterogeneity, serving instead as a critical starting point for subsequent functional and integrative analyses. - Source: PubMed
Publication date: 2026/02/16
Yang ZhiyaLi TingyangShen JiayunHuang YaoLei ChaoYu JiaruiMa ZhaochenLi YingZhang Ming - Antidepressant treatment remains a trial-and-error process: one-third of people with major depressive disorder (MDD) report inefficacy of first-line medications. Predictors of prescription patterns are needed to improve prescribing precision. - Source: PubMed
Walker AliciaMitchell Brittany LLin TianCrouse Jacob JAlbiñana ClaraYap Chloe XLynall Mary EllenLind Penelope ACipriani AndreaByrne Enda MMedland Sarah EMartin Nicholas GTaquet MaximeHickie Ian BWray Naomi R - A small percentage of people living with HIV (PLHIV) spontaneously regulate viral replication without suppressive antiretroviral treatment (ART) and are categorized into 'elite controllers' (EC, HIV-RNA < 50 c/mL) and 'viremic controllers' (VC, HIV-RNA between 50-10,000 c/ml). Some EC and VC may lose controller status in time. Here we provide extensive plasma proteomics to identify biomarkers and pathways related to spontaneous viral control and its long-term preservation among 36 EC and 147 VC (discovery) and 14 EC and 5 VC (validation). VC exhibited higher concentrations of CRTAM, LY9, and CD6 and lower concentrations of VAT1 compared to EC in both the discovery and validation cohort. Longitudinal analysis of pre- and post-ART samples (median follow-up: 5.3 years) revealed downregulation of various immune-related proteins in both EC and VC. Over a 17-year follow-up period, loss of viral control occurred in 31% of VC and 3% of EC. T-cell associated proteins (CRTAM, LY9, CD6), along with ICAM3, SH2D1A, C1QL2, and CNGB3, predicted loss of viral control years before its occurrence. Markers of chronic immune activation (sPD-L1, sCD25, IL-10, TGF-β, IFN-γ, and TNF-α) and systemic inflammation (TNF, IL-1β, IL-6, and sCD14) were not predictive. Our findings underscore the dynamic interplay between T cell function and viral replication in maintaining HIV control and identify key biomarkers that predict viral load surges. - Source: PubMed
Publication date: 2026/01/22
Vadaq NadiraGroenendijk Albert LDos Santos Jéssica CMehta KavitaWit Ferdinand W N MVos Wilhelm A J WBlaauw Martinus J Tvan Eekeren Louise ELambrechts LaurensRutsaert SofieNelwan Erni JXu Cheng-JianJoosten Leo A Bde Mast QuirijnMatzaraki Vasilikivan Lunzen JanRokx CasperVerbon AnneliesNetea Mihai GVandekerckhove Linosvan der Ven André J A M - Immune checkpoint blockade (ICB) therapy has transformed the treatment landscape for metastatic melanoma, yet predicting therapeutic response remains a significant challenge. This study hypothesizes that coordinated ligand-receptor (LR) interactions within the tumor microenvironment (TME) critically influence ICB efficacy and proposes that a novel LR pair-based signature score (LRPS) derived from on-treatment samples can predict clinical outcomes. In this study, we analyzed publicly available transcriptomic and clinical datasets comprising 144 patients and 168 on-treatment tumor samples from five independent cohorts (GEO: GSE120575, GSE115821, GSE168204; BioProject: PRJEB23709; dbGaP: phs001919.v1.p1; EGA: EGAD00001005738). We identified seven LR pairs (FLT3-FLT3LG, LY9-LY9, CD5-CD5, CD40LG-ITGA2B/ITGB3, APP-CD74, TNFRSF17-TNFSF13, FCER2-ITGAV/ITGB3) significantly associated with treatment outcomes. LRPS demonstrated strong predictive power, achieving an area under the ROC curve (AUC) exceeding 0.80 in four independent cohorts. Patients in the high-LRPS group exhibited higher ICB response rates (up to 76.2%) and significantly better progression-free survival (PFS) and overall survival (OS) compared with the low-LRPS group. In conclusion, we identified and verified an LRPS signature that provides a theoretical basis for applying such signatures derived from on-treatment tumor samples to predict therapeutic responses to ICB therapies. - Source: PubMed
Publication date: 2026/01/09
Zeng HuanchengZhang RendongJiang QiongzhiWu JundongZhuang ZheminFang Yutong