Monkey CD302 antigen(CD302) ELISA kit
- Known as:
- Monkey CD302 antigenic(CD302) Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- e09c1484
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Blue gene shanghai
- Gene target:
- Monkey CD302 antigen(CD302) ELISA kit
Related genes to: Monkey CD302 antigen(CD302) ELISA kit
- Gene:
- CD302 NIH gene
- Name:
- CD302 molecule
- Previous symbol:
- -
- Synonyms:
- DCL-1, KIAA0022, BIMLEC, CLEC13A
- Chromosome:
- 2q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-11
- Date modifiied:
- 2014-11-18
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- Glomerulonephritis (GN) is an immune-mediated kidney disorder that causes glomerular injury, progressive renal dysfunction, and end-stage kidney disease. Traditional treatments such as corticosteroids and immunosuppressants are limited by variable efficacy and severe adverse effects, highlighting the need for novel therapeutic targets and personalized strategies. We performed a systematic multi-omics Mendelian randomization (MR) analysis applying established proteomic and transcriptomic quantitative trait loci (pQTL/eQTL) resources to genome-wide association studies (GWAS) of four GN subtypes: acute, chronic, IgA nephropathy, and membranous nephropathy. Bayesian colocalization was used to strengthen causal inference, while independent replication and meta-analysis were conducted using the FinnGen cohort. Mouse knockout phenotypes, drug reposition, and computational pharmacology algorithm were applied to evaluate translational potential. Proteomic-wide MR revealed MTR as protective in chronic GN and HCK as a risk factor for membranous nephropathy, whereas CD302 and CDKN1B showed protective effects. Transcriptomic-wide MR identified candidate genes across GN subtypes: RECQL, BRSK2, and MGP in acute GN; AFM, CFHR5, and EPHB2 in chronic GN; IL6R, MBL2, and PRSS3 in IgA nephropathy; and TIMP4, HCK, and PEAR1 in membranous nephropathy. Bayesian colocalization analysis provided strong support for shared causal variants (PPH4 > 0.8) for HCK, CD302, TIMP4, PEAR1, PARP1, and FHIT. Replication and meta-analysis in the FinnGen cohort provided additional consistency across datasets, while downstream translational annotations highlighted IL6R, MBL2, C5, and CD55 as potential hub targets within immune and complement-related pathways. This integrative multi-omics study provides novel insights into the genetic architecture and therapeutic landscape of GN, identifying potential therapeutic targets that may inform precision nephrology and drug repurposing. Notably, most targets supported by colocalization, mouse knockout phenotypes, and drug repurposing evidence were predominantly identified in membranous nephropathy, suggesting a particularly tractable genetic and therapeutic architecture for this subtype. - Source: PubMed
Publication date: 2026/04/16
Li GuoqiangJianhan FuGu JiashuWang YinhuaiLiu JiachenYang DongZeng DianjieZhao Pengcheng - Proteome-wide risk models for lupus remain underexplored. We developed classification models to identify lupus from serum proteomic profiles. - Source: PubMed
Publication date: 2026/03/26
Hocaoǧlu MehmetDas JishnuSawalha Amr H - CD302 encodes a transmembrane glycoprotein involved in immune regulation via cell-extracellular matrix interactions. Its role in lung adenocarcinoma (LUAD) remains unexplored. This study investigates CD302's expression, clinical relevance, and functional mechanisms in LUAD. - Source: PubMed
Publication date: 2025/11/14
Wang KaiWang YaoLu TaoGao ManjunSong YongxiangChen ChengKe Xixian - A novel cell line (LYC-hK) was established from the head kidney of large yellow croaker (Larimichthys crocea), a major marine aquaculture fish species in China. The cell line has been continuously subcultured for over 100 passages and exhibits stable morphology, transitioning to fibroblast-like. Specifically, it exhibits a transition toward epithelium-like phenotype at high density. Karyotype analysis verified the stability of the diploid chromosome: approximately 50 % of the cells retained 48 chromosomes at the 120th passage. Functionally, LYC-hK displayed robust macrophage-like activity, including reactive oxygen species production upon stimulation with lipopolysaccharide (LPS) or phorbol myristate acetate (PMA), and efficient phagocytosis of Nocardia seriolae and Pseudomonas plecoglossicida, followed by time-dependent intracellular bacterial clearance. Gene expression profiling revealed high transcript abundance of macrophage-specific marker genes, including CD68, mpeg1, CD209/DC-SIGN, and CD302, alongside strong induction of the pro-inflammatory cytokines IL-1β and IL-8 upon bacterial challenge. Notably, high-level expression of the CD34 gene was also detected which implies that the LYC-hK might possess hematopoietic progenitor-like properties. Furthermore, successful transfection of the LYC-hK cells with the pEGFP-C2 plasmid confirmed the line's suitability for studies involving exogenous gene expression. Collectively, these findings indicate that LYC-hK is a stable macrophage-like cell line, providing a valuable in vitro model for studies of host-pathogen interactions and functional genomics in teleost fish. - Source: PubMed
Publication date: 2025/11/12
Liu YuTao ZhenYin FeiZhou Su-Ming - Hepatitis C virus (HCV) is an enveloped, positive-sense single-stranded RNA virus causing chronic infections in over 50 million people who are at risk of developing severe liver disease. Greater understanding of HCV pathogenesis and vaccine development has been hampered by the lack of a fully immunocompetent small-animal model permissive to infection. Rodents are resistant to HCV infection due to a variety of factors at the levels of entry and replication, many of which have been discovered within the past decade. We hypothesized that genetically altering these factors in mice would provide a host environment conducive to infection. Here, we present the generation and characterization of a series of mouse lines bearing humanized alleles for CD81, occludin, TRIM26, and CypA, the murine orthologs for which do not support HCV uptake and replication. Additionally, we knocked out CD302 and CR1L, which restrict HCV infection in mouse hepatocytes. Intravenously, inoculation of mice harboring some or all of these mutant alleles did not increase viremia. To ascertain that mouse adaptive immune responses do not rapidly clear any putative low-level viremia, we engrafted hepatocytes from these genetically complex lines into immunodeficient liver-injury strains. No cohort of mice presented with sustained HC viremia, although we detected low-level viremia in a subset of transplant-recipient mice. Collectively, although these mouse models did not support robust, sustained viremia, these mouse mutant lines represent the most genetically advanced mouse model of HCV infection and will provide an important platform for future genetic host adaptations and/or complementary viral adaptation approaches.IMPORTANCEHepatitis C virus (HCV) presents a significant threat to global health. Despite its prevalence worldwide, there remain significant knowledge gaps regarding immunopathogenesis, oncogenesis, and determinants for vaccine efficacy. This is due to the scarcity of small-animal models for HCV, a virus that only robustly infects human and chimpanzee hepatocytes. In this work, we genetically engineer mice to either humanize or remove several factors that are known to limit HCV infection in mice. We then expose these mice to HCV and assess whether they develop infection over time. To see whether the immune system impacts infection in these modified mice, we transplant liver cells from those mice into ones that lack immune cells and then assess their ability to develop HCV infection. While we did not succeed in generating a mouse that sustains robust viremia, these complex strains nevertheless represent an important platform for further model development. - Source: PubMed
Publication date: 2025/09/03
Schwoerer Michael PCarver SebastianCafiero Thomas RJoyce BradleyBerggren Keith ASuzuki SaoriHeller BrigitteO'Connell Aoife KGertje Hans PCrossland Nicholas APosfai EszterPloss Alexander