MOUSE ANTI HUMAN CD247 Azide Free

Price:
899 EUR
1078 USD
746 GBP
known as: MOUSE ANTI HUMAN CD247 Azide Free
Catalog number: genta-ABS0361
Product Quantity: 1 mg
Category:
Supplier: AbD

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Gene target: cd247

Related genes to: MOUSE ANTI HUMAN CD247 Azide Free

Symbol : cd247 NIH gene
chromosome : Un
description : CD247 molecule
type of gene : protein-coding
Other designations : t-cell surface glycoprotein CD3 zeta chain
Modification date : 2015-11-14

Related Pathways to: MOUSE ANTI HUMAN CD247 Azide Free

Gene about :CD247
Pathway :Hs T-Cell antigen Receptor (TCR) Signaling Pathway
CD247

Related product to: MOUSE ANTI HUMAN CD247 Azide Free

Related Articles about: MOUSE ANTI HUMAN CD247 Azide Free

Association of CD247 (CD3ζ) gene polymorphisms with T1D and AITD in the population of northern Sweden.

T1D and AITD are autoimmune disorders commonly occurring in the same family and even in the same individual. The genetic contribution to these disorders is complex making uncovering of susceptibility genes very challenging. The general aim of this study was to identify loci and genes contributing to T1D/AITD susceptibility. Our strategy was to perform linkage and association studies in the relatively genetically homogenous population of northern Sweden. We performed a GWLS to find genomic regions linked to T1D/AITD in families from northern Sweden and we performed an association study in the families to test for association between T1D/AITD and variants in previously published candidate genes as well as a novel candidate gene, CD247. - Source :PubMed

Primary T-cell immunodeficiency with functional revertant somatic mosaicism in CD247.

- Source :PubMed

Comprehensive Survey of miRNA-mRNA Interactions Reveals That Ccr7 and Cd247 (CD3 zeta) are Posttranscriptionally Controlled in Pancreas Infiltrating T Lymphocytes of Non-Obese Diabetic (NOD) Mice.

In autoimmune type 1 diabetes mellitus (T1D), auto-reactive clones of CD4+ and CD8+ T lymphocytes in the periphery evolve into pancreas-infiltrating T lymphocytes (PILs), which destroy insulin-producing beta-cells through inflammatory insulitis. Previously, we demonstrated that, during the development of T1D in non-obese diabetic (NOD) mice, a set of immune/inflammatory reactivity genes were differentially expressed in T lymphocytes. However, the posttranscriptional control involving miRNA interactions that occur during the evolution of thymocytes into PILs remains unknown. In this study, we postulated that miRNAs are differentially expressed during this period and that these miRNAs can interact with mRNAs involved in auto-reactivity during the progression of insulitis. To test this hypothesis, we used NOD mice to perform, for the first time, a comprehensive survey of miRNA and mRNA expression as thymocytes mature into peripheral CD3+ T lymphocytes and, subsequently, into PILs. Reconstruction of miRNA-mRNA interaction networks for target prediction revealed the participation of a large set of miRNAs that regulate mRNA targets related to apoptosis, cell adhesion, cellular regulation, cellular component organization, cellular processes, development and the immune system, among others. The interactions between miR-202-3p and the Ccr7 chemokine receptor mRNA or Cd247 (Cd3 zeta chain) mRNA found in PILs are highlighted because these interactions can contribute to a better understanding of how the lack of immune homeostasis and the emergence of autoimmunity (e.g., T1D) can be associated with the decreased activity of Ccr7 or Cd247, as previously observed in NOD mice. We demonstrate that these mRNAs are controlled at the posttranscriptional level in PILs. - Source :PubMed

Natural killer cell hyporesponsiveness and impaired development in a CD247-deficient patient.

- Source :PubMed

Response to Comment on "A Novel Thymoma-Associated Immunodeficiency with Increased Naive T Cells and Reduced CD247 Expression".

- Source :PubMed

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