TRBV5-1: A Potential Drug Target and Biomarker for T Cell Receptor Beta Variable 5-1

Target Name: TRBV5-1

NCBI ID: G28614

TRBV5-1

Other Name(s): T cell receptor beta variable 5-1 | TCRBV5S1A1T | TRBV51 | TCRBV5S1

TRBV5-1: A Potential Drug Target and Biomarker for T Cell Receptor Beta Variable 5-1

Abstract:

T cell receptor beta variable 5-1 (TRBV5-1) is a cell surface protein that plays a crucial role in T cell activation and regulation. The TRBV5-1 gene has been identified as a potential drug target and biomarker for various diseases, including cancer, autoimmune disorders, and neurodegenerative diseases. This article summarizes the current understanding of TRBV5-1, its potential drug target status, and its potential as a biomarker for disease diagnosis and treatment.

Introduction:

T cells are a vital part of the immune system, and their activation and regulation by T cell receptor beta variable 5-1 (TRBV5-1) is critical for their proper function. TRBV5-1 is a transmembrane protein that consists of an extracellular portion and an intracellular portion. The intracellular portion of TRBV5-1 contains a N-terminal transmembrane domain, a coiled-coil region, and a C-terminal cytoplasmic domain. The cytoplasmic region of TRBV5-1 contains a single splice variant gene that encodes a protein with 115 amino acid residues.

Disease association:

TRBV5-1 has been associated with various diseases, including cancer, autoimmune disorders, and neurodegenerative diseases. TRBV5-1 has been shown to play a critical role in T cell activation and regulation, and its dysfunction has been implicated in the development and progression of these diseases.

Drug targeting:

TRBV5-1 has been identified as a potential drug target for various diseases. One of the main reasons for its potential as a drug target is its unique structure and function. TRBV5-1 has a unique N-terminal transmembrane domain that is involved in the formation of a complex with other proteins. This domain is also involved in the regulation of TRBV5-1 function, including its interactions with intracellular signaling pathways.

TRBV5-1 has also been shown to have a kinase-like activity, which suggests that it may be a potential target for inhibitors of protein kinases. Additionally, TRBV5-1 has been shown to interact with several signaling pathways, including the PI3K/Akt signaling pathway, which is involved in the regulation of cell survival and proliferation.

Biomarker potential:

TRBV5-1 has also been shown to be a potential biomarker for several diseases. One of the main reasons for its potential as a biomarker is its expression and stability in different tissues and cells. TRBV5-1 has been shown to be expressed in a variety of tissues, including T cells, B cells, and macrophages. Additionally, TRBV5-1 has been shown to have a stable expression level in these tissues, which suggests that it may be a potential biomarker for disease diagnosis and treatment.

Another reason for TRBV5-1's potential as a biomarker is its expression pattern in disease-related tissues. TRBV5-1 has been shown to be expressed in various disease-related tissues, including cancer, autoimmune disorders, and neurodegenerative diseases. This suggests that TRBV5-1 may be a potential biomarker for these diseases, and that its dysfunction may contribute to the development and progression of these diseases.

Conclusion:

In conclusion, TRBV5-1 is a cell surface protein that has been associated with various diseases. Its unique structure and function, as well as its potential as a drug target and biomarker, make it an attractive target for research into the development and treatment of these diseases. Further research is needed to fully understand the role of TRBV5-1 in disease progression and to develop effective treatments.

Protein Name: T Cell Receptor Beta Variable 5-1

Functions: V 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)

The "TRBV5-1 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about TRBV5-1 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
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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