TRBJ2-5: A Potential Drug Target and Biomarker for T Cell Receptor Beta Joining 2-5

Target Name: TRBJ2-5

NCBI ID: G28624

TRBJ2-5

Other Name(s): T cell receptor beta joining 2-5 | TRBJ25 | TCRBJ2S5

TRBJ2-5: A Potential Drug Target and Biomarker for T Cell Receptor Beta Joining 2-5

Abstract:

T cell receptor (TCR) beta joining 2-5 (TRBJ2-5) is a critical regulator of T cell activation and proliferation. Abnormalities in TRBJ2-5 signaling have been implicated in a variety of autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, and T cell acute lymphoblastic leukemia. In this article, we review the current understanding of TRBJ2-5 function, its potential as a drug target, and its potential as a biomarker for tracking disease progression.

Introduction:

T cells are a crucial immune cell that play a critical role in defending against infections and diseases. T cell receptor (TCR) beta joining 2-5 (TRBJ2-5) is a key regulator of T cell activation and proliferation. TRBJ2-5 is a cytoplasmic protein that is involved in the formation of the T cell receptor complex, which is responsible for the recognition of antigens and the activation of T cells.

TRBJ2-5 function:

TRBJ2-5 is a cytoplasmic protein that is composed of two main subunits: TRBJ2 and TRBJ2-5 itself. TRBJ2 is a 21-kDa protein that contains a nucleotide-binding oligomerization domain (NBD) and a carboxy-terminal domain (CTD). TRBJ2-5 is a 19-kDa protein that contains a NBD and a CTD.

In T cells, TRBJ2 is involved in the formation of the T cell receptor complex by interacting with the scaffold protein PDZ1. TRBJ2-5, on the other hand, is involved in the regulation of T cell activation and proliferation by interacting with the protein PDZL1.

TRBJ2-5 as a drug target:

TRBJ2-5 has been identified as a potential drug target due to its involvement in T cell regulation. Several studies have shown that inhibiting TRBJ2-5 signaling can enhance the activity of adoptive T cell memory responses and improve the generation of memory T cells. In addition, TRBJ2-5 has been shown to play a role in the regulation of T cell proliferation and differentiation, and its dysregulation has been implicated in the development of several autoimmune diseases.

TRBJ2-5 as a biomarker:

TRBJ2-5 has also been shown to be a potential biomarker for tracking disease progression in several autoimmune diseases. For example, studies have shown that TRBJ2-5 levels are elevated in individuals with rheumatoid arthritis (RA) and multiple sclerosis (MS), and that these individuals have decreased levels of T cell function. Additionally, individuals with RA and MS have lower levels of TRBJ2-5 compared to healthy individuals.

Conclusion:

TRBJ2-5 is a critical regulator of T cell activation and proliferation, and its dysregulation has been implicated in a variety of autoimmune diseases. As a potential drug target, TRBJ2-5 has the potential to enhance the activity of adoptive T cell memory responses and improve the generation of memory T cells. As a biomarker, TRBJ2-5 may be useful for tracking disease progression in autoimmune diseases. Further research is needed to fully understand the role of TRBJ2-5 in T cell regulation and its potential as a drug target and biomarker.

Protein Name: T Cell Receptor Beta Joining 2-5

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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The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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