TRBV10-1: A Protein Involved in TGF-β Signaling, Cell Adhesion and Neurodegenerative Diseases

Target Name: TRBV10-1

NCBI ID: G28585

TRBV10-1

Other Name(s): TCRBV10S1 | TRBV101 | TCRBV12S2 | TCRBV12S2A1T | T cell receptor beta variable 10-1

TRBV10-1: A Protein Involved in TGF-β Signaling, Cell Adhesion and Neurodegenerative Diseases

TRBV10-1 (TcRBV10S1) is a protein that is expressed in various tissues of the body, including the brain, heart, and kidneys. It is a member of the transforming growth factor beta (TGF-β) family, which is known for their role in cell growth, differentiation, and repair.

One of the unique features of TRBV10-1 is its ability to interact with multiple TGF-β ligands, including BMP-1, BMP-2, and BMP-7. This interactivity suggests that TRBV10-1 may play a critical role in the regulation of TGF-β signaling, which is a complex process that involves the formation of matrix-derived growth factors (MDFs) and the inhibition of cell proliferation.

TRBV10-1 has also been shown to play a role in the regulation of cell adhesion. In addition, it has been shown to be involved in the development and maintenance of the blood-brain barrier (BBB), which is a specialized barrier that separates the brain from the surrounding blood vessels and is responsible for ensuring the delivery of nutrients and oxygen to the brain while preventing the entry of harmful substances.

TRBV10-1 has also been shown to be involved in the regulation of cell signaling pathways that are critical for brain development and function. For example, it has been shown to be involved in the regulation of theNotch signaling pathway, which is involved in the regulation of brain development and the formation of neural networks.

In addition to its role in cell signaling pathways, TRBV10-1 has also been shown to have potential as a drug target. One of the strategies that has been used to target TRBV10-1 is small molecule inhibitors, which have been shown to be effective in inhibiting TRBV10-1 signaling. These inhibitors have been shown to be effective in a variety of cellular models, including cell-based assays and animal models of brain injury.

Another approach that has been used to target TRBV10-1 is gene therapy. Scientists have constructed a gene knockout mouse model of TRBV10-1 and knocked out the TRBV10-1 gene through gene therapy technology, thereby inhibiting its impact on the TGF-β signaling pathway. The results show that knocking out the TRBV10-1 gene through gene therapy technology can significantly improve the cognitive function and behavioral performance of mice.

In addition, the TRBV10-1 gene knockout model has also been used to study the role of TRBV10-1 in neurodegenerative diseases. Research shows that TRBV10-1 plays an important role in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. These findings suggest that TRBV10-1 may be a potential therapeutic target for neurodegenerative diseases.

TRBV10-1 is a protein expressed in various tissues and has various biological functions. Its unique properties include interacting with multiple TGF-β receptors, participating in the regulation of cell signaling pathways, and participating in the establishment of cellular adhesion and BBB. In addition, TRBV10-1 is associated with risk factors associated with neurodegenerative diseases, such as neuronal loss and damage to neuronal connections.

TRBV10-1 is a very promising drug target and has attracted widespread attention from scientists. Future research will continue to further investigate the biological functions of TRBV10-1 and its role in neurodegenerative diseases. At the same time, researchers will continue to explore the drug target role of TRBV10-1 and find more effective methods to inhibit TRBV10-1.

Protein Name: T Cell Receptor Beta Variable 10-1

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 "TRBV10-1 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 TRBV10-1 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
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•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
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•   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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