TRBV5-7: A Potential Drug Target and Biomarker (G28608)

Target Name: TRBV5-7

NCBI ID: G28608

TRBV5-7

Other Name(s): TRBV57 | TCRBV5S7P | T cell receptor beta variable 5-7 (non-functional) | TCRBV5S7

TRBV5-7: A Potential Drug Target and Biomarker

TRBV5-7, also known as Tissue Response Biomarker 5-7, is a protein that is expressed in various tissues of the body, including the lungs, heart, kidneys, and liver. It is a member of the transforming growth factor beta (TGF -尾) family, which is involved in cell growth, differentiation, and survival. TRBV5-7 has been shown to play a role in the development and progression of a variety of diseases, including cancer, cardiovascular disease, and neurodegenerative diseases. As a As a result, it has become a focus of interest for researchers looking for new treatments.

One of the key reasons why TRBV5-7 has potential as a drug target is its involvement in the TGF-β signaling pathway. TGF-β is a cytokine that plays a vital role in the development and maintenance of tissues, and it is involved in the regulation of cell growth, differentiation, and survival. Activated TGF-β signaling has been implicated in the development of many diseases, including cancer, neurodegenerative diseases, and cardiovascular disease.

Studies have shown that TRBV5-7 is involved in TGF-β signaling in a variety of ways. For example, it has been shown to be a direct target of TGF-β, and it has been shown to regulate the activity of TGF-β signaling pathway in various tissues. Additionally, TRBV5-7 has been shown to play a role in the regulation of cell proliferation and survival, which are important steps in the development and progression of many diseases.

Another reason why TRBV5-7 has potential as a drug target is its involvement in the regulation of inflammation. Chronic inflammation is a major risk factor for the development of many diseases, including cardiovascular disease and neurodegenerative diseases. TRBV5-7 has been shown to be involved in the regulation of inflammation in various tissues, and it has been shown to play a role in the regulation of immune responses.

In addition to its involvement in TGF-β signaling and inflammation, TRBV5-7 has also been shown to be involved in the regulation of cell adhesion. Cell adhesion is the process by which cells stick together and form tissues, and it is an important step in the development and progression of many diseases. TRBV5-7 has been shown to play a role in the regulation of cell adhesion in various tissues, and it has been shown to be involved in the development of cancer.

Despite its potential as a drug target, TRBV5-7 is still an relatively unstudied protein. There is currently limited research on the mechanisms of TRBV5-7, and there are few potential drug targets that have been identified. However, research into TRBV5-7 is an exciting area of 鈥嬧?媠tudy, and it has the potential to lead to new treatments for a variety of diseases.

In conclusion, TRBV5-7 is a protein that has been shown to be involved in the TGF-β signaling pathway, inflammation, and cell adhesion. Its potential as a drug target is based on its involvement in these processes, as well as its involvement in the regulation of cell growth and survival. Further research is needed to fully understand the mechanisms of TRBV5-7, and to identify potential drug targets. If successful, TRBV5-7 may become a valuable tool for the development of new treatments for a variety of diseases.

Protein Name: T Cell Receptor Beta Variable 5-7 (non-functional)

Functions: Probable non-functional open reading frame (ORF) of V region of the variable domain of T cell receptor (TR) beta chain (PubMed:24600447). Non-functional ORF generally cannot participate in the synthesis of a productive T cell receptor (TR) chain due to altered V-(D)-J or switch recombination and/or splicing site (at mRNA level) and/or conserved amino acid change (protein level) (PubMed:9619395). 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 "TRBV5-7 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 TRBV5-7 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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