TRBJ1-3: A Potential Drug Target in Immunology (G28633)

Target Name: TRBJ1-3

NCBI ID: G28633

TRBJ1-3

Other Name(s): T cell receptor beta joining 1-3 | TCRBJ1S3 | TRBJ13

TRBJ1-3: A Potential Drug Target in Immunology

TRBJ1-3, also known as T cell receptor beta joining 1-3, is a protein that is expressed in the T cells of the immune system. It plays a crucial role in the process of immune response, specifically in the regulation of T cell activity. TRBJ1-3 has been identified as a potential drug target and is the focus of ongoing research in the field of immunology.

The immune system is a critical component of the body's defense against infection and disease. T cells, a type of immune cell, are responsible for cell-mediated immunity. They are able to recognize and respond to the presence of foreign or abnormal substances in the body. TRBJ1-3 is a key regulator of T cell activity, and its function is essential for the development and maintenance of a healthy immune system.

TRBJ1-3 is a transmembrane protein that is expressed in the T cells of the immune system. It is composed of two distinct that are held together by disulfide bonds. The two chains have different functions, with the N-terminus of one chain containing chains a nucleotide exchange domain (NED) and the C-terminus containing a carboxylic acid residue (CA) and a conserved structural domain (CSD). The NED is responsible for the formation of a disulfide bond, while the CSD is involved in the regulation of the protein's stability and interactions with other molecules.

TRBJ1-3 is involved in the regulation of T cell receptor (TCR) function. TCR is a protein that is expressed on the surface of T cells and is responsible for cell-mediated immunity. It is composed of a variable region, which contains the T cell receptor alpha chain, and a constant region, which contains a conserved framework that is involved in receptor recognition. TRBJ1-3 is responsible for the regulation of TCR function by interacting with the NED of TCR.

TRBJ1-3 plays a critical role in the regulation of T cell activation and proliferation. It is able to inhibit the activation and proliferation of T cells by interacting with the NED of TCR. This interaction between TRBJ1-3 and TCR is important for the regulation of T cell activity and is a potential drug target.

TRBJ1-3 is also involved in the regulation of T cell death. T cells are a vital part of the immune system and play a critical role in the regulation of inflammation and infection. However, they are also prone to apoptosis, which is the process by which cells self-destruct. TRBJ1-3 is involved in the regulation of T cell death by interacting with the CA and CSD of TCR. This interaction between TRBJ1-3 and TCR is important for the regulation of T cell life cycle and is a potential drug target.

In conclusion, TRBJ1-3 is a protein that is expressed in the T cells of the immune system and plays a crucial role in the regulation of T cell activity. It is a potential drug target and is the focus of ongoing research in the field of immunology. Further studies are needed to fully understand the function of TRBJ1-3 and its potential as a drug.

Protein Name: T Cell Receptor Beta Joining 1-3

Functions: J region of the variable domain of T cell receptor (TR) beta chain that participates in the antigen recognition (PubMed:24600447). Alpha-beta T cell receptors are antigen specific receptors which are essential to the immune response and are present on the cell surface of T lymphocytes. Recognize peptide-major histocompatibility (MH) (pMH) complexes that are displayed by antigen presenting cells (APC), a prerequisite for efficient T cell adaptive immunity against pathogens (PubMed:25493333). Binding of alpha-beta TR to pMH complex initiates TR-CD3 clustering on the cell surface and intracellular activation of LCK that phosphorylates the ITAM motifs of CD3G, CD3D, CD3E and CD247 enabling the recruitment of ZAP70. In turn ZAP70 phosphorylates LAT, which recruits numerous signaling molecules to form the LAT signalosome. The LAT signalosome propagates signal branching to three major signaling pathways, the calcium, the mitogen-activated protein kinase (MAPK) kinase and the nuclear factor NF-kappa-B (NF-kB) pathways, leading to the mobilization of transcription factors that are critical for gene expression and essential for T cell growth and differentiation (PubMed:23524462). The T cell repertoire is generated in the thymus, by V-(D)-J rearrangement. This repertoire is then shaped by intrathymic selection events to generate a peripheral T cell pool of self-MH restricted, non-autoaggressive T cells. Post-thymic interaction of alpha-beta TR with the pMH complexes shapes TR structural and functional avidity (PubMed:15040585)

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