TRBJ2-2: A Potential Drug Target and Biomarker for T Cell Receptor Beta Joining 2-2

Target Name: TRBJ2-2

NCBI ID: G28628

TRBJ2-2

Other Name(s): T cell receptor beta joining 2-2 | TCRBJ2S2 | TRBJ22

TRBJ2-2: A Potential Drug Target and Biomarker for T Cell Receptor Beta Joining 2-2

T cells are a crucial immune cell that play a major role in protecting the body against infection and disease. T cell receptor (TCR) beta joining 2-2 is a protein that is expressed on the surface of T cells and is involved in the process of T cell activation and proliferation. Researchers have been investigating TRBJ2-2 as a potential drug target and biomarker for various autoimmune diseases, including rheumatoid arthritis, lupus, and multiple sclerosis.

The TRBJ2-2 protein is composed of two subunits, TRBJ2 and TRBJ2-1. TRBJ2 is a 21-kDa protein that contains a N-terminal transmembrane domain, a catalytic domain, and a C-terminal T cell receptor (TCR) binding domain . TRBJ2-1 is a 19-kDa protein that contains a N-terminal transmembrane domain, a catalytic domain, and a C-terminal TCR binding region. TRBJ2 and TRBJ2-1 are held together by a disulfide bond, which is a structural feature that contributes to the stability and stability of the protein.

TRBJ2-2 is involved in the process of T cell receptor beta joining 2-2. This is the site where the TCR binds to the antigen and activates the T cell. TRBJ2-2 plays a crucial role in regulating the amount of beta joining that occurs, as well as the speed at which it occurs.

Research has shown that TRBJ2-2 is involved in the regulation of T cell activation and proliferation. Studies have shown that TRBJ2-2 plays a role in the development of autoimmune diseases, including rheumatoid arthritis, lupus, and multiple sclerosis. For example, researchers have shown that individuals with rheumatoid arthritis have lower levels of TRBJ2-2 in their T cells compared to individuals without the disease.

In addition to its involvement in autoimmune diseases, TRBJ2-2 has also been shown to be involved in cancer. Studies have shown that TRBJ2-2 is often overexpressed in various types of cancer, including breast, lung, and ovarian cancer. This suggests that TRBJ2-2 may be a potential biomarker for cancer and could be a target for cancer therapies.

TRBJ2-2 has also been shown to be involved in the regulation of inflammation. Studies have shown that TRBJ2-2 is involved in the production of pro-inflammatory cytokines, such as TNF-alpha, IL-1, and IL-6. This suggests that TRBJ2-2 may be involved in the development of inflammatory diseases, such as rheumatoid arthritis and lupus.

In conclusion, TRBJ2-2 is a protein that is expressed on the surface of T cells and is involved in the process of T cell receptor beta joining 2-2. Studies have shown that TRBJ2-2 is involved in the regulation of T cell activation and proliferation, as well as the development of autoimmune diseases and cancer. In addition, TRBJ2-2 has also been shown to be involved in the regulation of inflammation. Based on these findings, TRBJ2-2 may be a potential drug target and biomarker for various autoimmune diseases, including rheumatoid arthritis, lupus, and multiple sclerosis, as well as cancer. Further research is needed to fully understand the role of TRBJ2-2 in these diseases and to develop effective therapies based on this protein.

Protein Name: T Cell Receptor Beta Joining 2-2

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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