CD3Z Mouse Monoclonal Antibody
- Known as:
- CD3Z Mouse Monoclonal Antibody
- Catalog number:
- BIN-000919-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CD3Z Mouse Monoclonal Antibody
Related genes to: CD3Z Mouse Monoclonal Antibody
- Gene:
- CD247 NIH gene
- Name:
- CD247 molecule
- Previous symbol:
- CD3Z
- Synonyms:
- CD3H, CD3Q
- Chromosome:
- 1q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-06
- Date modifiied:
- 2019-04-23
Related products to: CD3Z Mouse Monoclonal Antibody
Related articles to: CD3Z Mouse Monoclonal Antibody
- In genome-wide survival association studies, time-to-event (TTE) phenotypes are often underutilized due to the challenges of large-scale multiple testing under linkage disequilibrium and heavy censoring. We propose Cox-MK, a novel genome-wide survival analysis framework that integrates knockoff statistics with the saddlepoint approximation (SPA), enabling SNP-level false discovery rate (FDR) control in biobank-scale studies. Simulation studies and real-data applications of UK Biobank data for both common and rare variants demonstrate that the proposed method achieves higher statistical power and well-calibrated FDR control compared with existing approaches. Compared with SPACox, Cox-MK identifies additional candidate genes for TTE traits. Specifically, it detects 47 additional SNPs mapped to 28 genes for asthma and 16 additional SNPs mapped to 12 genes for ischemic heart disease, including CD247 for asthma and EDNRA for ischemic heart disease. Overall, Cox-MK provides an effective tool for prioritizing putative causal variants underlying complex survival phenotypes. - Source: PubMed
Publication date: 2026/05/13
Hu LinYang ChenTang ZihuanYan JingminCheng HuayingBao LeiJi JiadongMa ShiyangZhang Tao - Idiopathic pulmonary fibrosis (IPF) is a progressive fibrotic lung disease that has increasingly been associated with dysregulated mitochondrial quality control and dynamics. However, the molecular mechanisms underlying these alterations remain incompletely understood. This study aimed to systematically identify and validate candidate biomarkers related to mitochondrial dynamics in IPF and to characterize their cell-type specificity and putative regulatory relationships. - Source: PubMed
Publication date: 2026/04/23
Wang YongbinCheng PengMeng ZixiangZhang YingLi YanFeng Feifei - This study aimed to identify key molecular signatures and therapeutic targets in early sepsis through integrated bioinformatics analysis. - Source: PubMed
Publication date: 2026/03/23
Gai XiaoweiLi YaqingWang YananGao DanWu ShanshanGeng YananZhang JiaminYao MinghuiYao GaiqiWang Qiuyan - Dysregulation of the CARD11-BCL10-MALT1 (CBM) complex is associated with a group of inborn errors of immunity termed “CBM-opathies,” which encompass a spectrum of clinical manifestations including combined immunodeficiency, autoimmune inflammation, atopic disorders, and lymphoproliferation. In this study, we identified novel compound heterozygous variants in the CBM complex in a patient with a family history of immune dysfunction. The patient inherited the variants CARD11 p.K215N and MALT1 p.K543R/p.M732T from asymptomatic carrier parents. Phenotypically, the patient exhibited a developmental arrest of B lymphocytes at the transitional/naïve B cell stage, accompanied by activation of virus-response pathways. Impaired development of T follicular helper cells was linked to defective germinal center formation and agammaglobulinemia. Furthermore, the patient showed expansion of T peripheral helper cells and a deficiency in regulatory T cells, both associated with autoimmunity and colitis. In vitro studies confirmed an imbalance in Tph/Tfh cell differentiation. Single-cell RNA sequencing further revealed a deficiency in B cell development and an enriched population of pro-inflammatory CD3dimCD4−CD8−CD247+ T cells, functionally enriched in the MAPK signaling pathway. Mechanistically, the MALT1 K543R and M732T variants attenuated MALT1’s enzymatic activity and compromised its protein stability, while the CARD11K215N variant disrupted CARD11-mediated promotion of BCL10 filament formation. We demonstrated that these three variants act synergistically to impair NF-κB activation. Specifically, CARD11K215N cooperates with the co-pathogenic MALT1M732T and the modifier variant MALT1K543R to destabilize the functional integrity of the CBM complex, thereby driving the patient’s phenotype. In summary, our study provides new insights into the pathogenesis of autoimmune inflammatory disorders within the spectrum of CBM-opathies and reveals a potential role for the CBM complex in regulating the balance between T peripheral helper and T follicular helper cells. - Source: PubMed
Publication date: 2026/03/26
Li RuiSun XiaochenBao WeiYu HaolanDan YuQingWu ChunmeiMa YanYin HanlinLin WanyiLu LiangjingFu QiongYang Chenghua - Celiac disease (CD) is highly prevalent in the wheat eating population of India. While HLA-DQ genotype is the strongest genetic determinant of CD, other genetic factors are likely contribute to genesis of CD. In this case-control study, we determined the frequencies of single nucleotide polymorphisms (SNP) in non-HLA candidate genes that influence the development of CD. DNA obtained from peripheral blood of 376 patients with CD and 736 controls was used for the studies. Fifty-one candidate gene polymorphisms were identified for evaluation. Competitive allele-specific polymerase chain reactions were designed to genotype biallelic SNPs at the selected loci. The genotype and allelotype was determined using KASP genotyping technology in a real-time PCR instrument. Eighteen of the 51 SNPs tested associated strongly with CD. The strongest association was found with the HLA DQ2.5 haplotype. HLA DQ2.2 haplotype and HLA-DQ8 haplotype were also strongly associated with CD. Non-HLA genes that were significantly associated with CD included those associated with T cell receptor signaling and T cell activation - CD247, CD80, CD28, PRKCQ, TNFAIP3, UBASH3 and ARHGAP31; genes involved in inflammatory cell migration - CCR3 and CCR4; those involved in epithelial protection - GATD3, PARK7 and INAVA (C1orf106); and those influencing RNA - DDX6 and PUS10. We concluded that the non-HLA genes associated with CD in this Indian population were mostly those associated with molecules involved in the T cell receptor signaling pathway downstream to HLA-DQ2/8, which lead to immune and subsequent inflammatory activation. - Source: PubMed
Publication date: 2026/03/25
Ramakrishna Balakrishnan SSingh AlkaSrinivasan PugazhendhiVenugopal GiriprasadGayathri RAhmed AnamSingh NidhiDutta SangitanjanAhuja VineetMakharia Govind K