MS4A3 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- MS4A3 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100063
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- MS4A3 antibody Polyclonal Antibodies Primary antibodies
Related genes to: MS4A3 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- MS4A3 NIH gene
- Name:
- membrane spanning 4-domains A3
- Previous symbol:
- CD20L
- Synonyms:
- HTM4
- Chromosome:
- 11q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-14
- Date modifiied:
- 2016-01-20
Related products to: MS4A3 antibody Polyclonal Antibodies Primary antibodies
Related articles to: MS4A3 antibody Polyclonal Antibodies Primary antibodies
- Colorectal cancer (CRC) is one of the most common malignant tumors worldwide. Patients with different immunophenotypes of CRC could achieve different effect of immunotherapy and yield different prognosis. With the advancement of bioinformatics, multi-omics analysis of the variations at both genomics and epigenomics levels helps a lot to provide a molecular basis for immunophenotype. Gene expression and clinical data of CRC patients were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). We calculated Spearman correlation of CD274 (programmed cell death ligand-1, PD-L1) and IFNG (interferon gamma, IFN-γ) expressions with immune cell fraction, and screened different immune cell types with CD274 and IFNG by Lasso regression analysis. Multi-omics analysis was exploited to screen out candidate genes with differential in genetic and epigenetic landscapes between two CRC subtypes with the greatest difference in immune infiltration. Finally, a risk scoring model was established and the role of candidate genes in prognosis and oncoimmunology was evaluated at the pan-cancer level. Two CRC types (cluster A and cluster B) including five subtypes (subclusters A1, A2, B1, B2A, and B2B) were identified by unsupervised clustering analysis. Somatic mutations, CNVs, and DNA methylation differed between subcluster A2 and B2, and analysis of DEGs correlated with CRC immune phenotypes identified FUT9 and MS4A3 as key genes related to CRC immune-phenotypes and prognosis. Furthermore, FUT9 was validated to act as a key gene related to CRC immune escape in vitro. The present study established a risk model for CRC immunophenotyping and prognosis, and highlighted the significance of FUT9 and MS4A3 in oncoimmunology of CRC. - Source: PubMed
Publication date: 2026/03/23
Zhu MinjingDong HaibeiHu YanyanXu XiFang Zejun - Transcriptomic analysis of blood cells can reveal key elements of the dysregulated host response in sepsis and spur biomarker and mechanism identification. We hypothesized that sepsis nonsurvivors exhibit a distinct transcriptional signature in whole blood that reflects insights to sepsis mortality. We conducted a prospective observational cohort study of 161 critically ill sepsis patients. Whole blood RNA was collected within 24 hours of intensive care unit admission. Gene expression levels were measured using microarrays and changes in gene levels were compared between 30-day nonsurvivors and survivors, adjusting for age, sex, and neutrophil count. Pathway overrepresentation analysis and weighted gene co-expression analysis were performed to identify biological pathways and gene co-expression groups, respectively, associated with sepsis mortality. Gene- and pathway-based results were compared to findings in an independent cohort of 479 sepsis patients with 28-day mortality data. Thirty-day mortality in the enrolled sepsis cohort was 37% (60 of 161 patients). We identified 1,106 differentially expressed genes in nonsurvivors (Benjamini-Hochberg-adjusted p-value <0.05), including several neutrophil-related genes (CEACAM8, ELANE, PRTN3, MPO, CEACAM6, DEFA4, MS4A3) with expression levels over 1.8 times higher in nonsurvivors despite adjusting for neutrophil counts. The neutrophil degranulation pathway was prominent based on its overrepresentation in 1) differentially expressed genes in both cohorts, 2) overrepresentation by gene set enrichment analysis, and 3) four of the six gene co-expression groups correlated with sepsis mortality. Our findings highlight the involvement of neutrophil degranulation genes in sepsis mortality, prompting further study to better understand whether they constitute a modifiable target. - Source: PubMed
Publication date: 2026/02/21
Giannini Heather MKan MengyuanCosgriff Christopher VMorley Michael PMiano Todd ANarayanan NishaIttner Caroline A GTurner Alexandra PEsperanza Mika PErlich Matthew COniyide OluwatosinAnderson Brian JJones Tiffanie KFeng RuiReilly John PHimes Blanca EShashaty Michael G SMeyer Nuala J - Genome-wide association studies (GWASs) have identified thousands of putative disease-causing variants with unknown regulatory effects. Efforts to connect these variants with splicing quantitative trait loci (sQTLs) have provided functional insights, yet sQTLs reported by existing methods cannot explain many GWAS signals. We show that current sQTL modeling approaches can be improved by considering alternative splicing representation, model calibration, and covariate integration. We then introduce MAJIQTL, a pipeline for sQTL discovery. MAJIQTL includes two statistical methods: a weighted multiple-testing approach for sGene discovery and a model for sQTL effect-size inference to improve variant prioritization. By applying MAJIQTL to GTEx, we find significantly more sGenes harboring sQTLs with functional significance. Notably, our analysis implicates the variant rs528823 in Alzheimer disease. Using antisense oligonucleotides, we test this variant's effect by blocking the implicated YBX3 binding site, leading to exon skipping in MS4A3. - Source: PubMed
Publication date: 2025/11/12
Wang DavidGazzara Matthew RJewell SanWales-McGrath Benjamin DYang KevinBrown Christopher DChoi Peter SBarash Yoseph - Traumatic brain injury (TBI) is an environmental risk factor for dementia and long-term neurological deficits, posing a significant public health challenge. TBI-induced neuroinflammation involves both brain-resident microglia and peripheral monocyte-derived macrophages (MDMs). Previous research has shown that MDMs contribute to the development of long-term memory deficits, yet their long-term behavior following brain infiltration remains unclear. To address this, our study uses two complementary fate-mapping mouse lines, CCR2-creERT2 and Ms4a3-cre, for precise and lasting tracking of MDMs in vivo. Here we show that MDMs persist in the brain for at least 8 months post-TBI in both male and female mice. MDMs retain phagocytic activity for at least 30 days post-TBI, remain transcriptionally distinct from microglia, and display a gene expression profile associated with aging and disease. Moreover, we identify a core transcriptomic signature of MDMs shared across various mouse models and brain perturbations, which is also enriched in the brain myeloid cells of male subjects with TBI and Alzheimer's disease patients. These findings enhance our understanding of MDMs' dynamics after TBI and inform future targeted myeloid-based therapies. - Source: PubMed
Publication date: 2025/10/07
Paladini Maria SerenaYang Benjamin ATorkenczy Kristof AFrias Elma SFeng XiKrukowski KarenSit ReneMorri MaurizioLam WendyPedoia ValentinaTyanova StefkaColonna MarcoNolan Amber LRosi Susanna - Most of the mast cells (MCs) in connective tissues, such as skin, are long-lived embryonic-derived immune cells that play important roles in host defense and in various immunological diseases, including allergies. Their embryonic origin and ontogeny remain to be fully studied since several overlapping waves of embryonic hematopoiesis have been reported to give rise to these cells. Here, combining single-cell RNA sequencing and new genetic fate mapping models, we identified a Cpa3-expressing population sequentially appearing in the yolk sac, fetal liver, and peripheral tissues which gives rise to dermal MCs during embryonic days 11.5 to 14.5. Using in vitro differentiation and in vivo transplantation assays, we identified a Ter119F4/80CD45CD117CD16/32CD135CD115Ly6CCD34 population as potential fetal liver MC precursors (MCPs). Fate mapping with Cpa3 and Zbtb16 models, as well as the granulocyte-monocyte progenitors (GMPs) fate mapping Ms4a3 and Elane models, demonstrated that MCs arise from Cpa3 precursors rather than Ms4a3 or Elane GMPs. A corresponding population with a similar developmental trajectory was also identified in human early yolk sac and fetal liver, suggesting a conserved MC developmental program across species. These findings reveal a distinct developmental path of skin MCs in embryos, permitting future functional studies in immunity and development. - Source: PubMed
Publication date: 2025/05/22
Ma WeiChen HuifangGao FeiZhao HanWu NingboZhang ShuangyanZhu YiwenXu ZijianLan YuLiu BingYe YouqiongLiu ZhaoyuanGinhoux FlorentSu Bing