TRBV6-7: A Non-Coding RNA Molecule as A Potential Drug Target for Neurodegenerative Diseases

Target Name: TRBV6-7

NCBI ID: G28600

TRBV6-7

Other Name(s): TCRBV6S7 | TCRBV13S8P | T cell receptor beta variable 6-7 (non-functional) | TRBV67

TRBV6-7: A Non-Coding RNA Molecule as A Potential Drug Target for Neurodegenerative Diseases

TRBV6-7 (TcRBV6S7) is a non-coding RNA molecule that has been identified as a potential drug target (also known as biomarker) in the field of neurodegenerative diseases, including Alzheimer's disease. The TRBV6-7 molecule is a key regulator of the translation of mRNAs in the brain, and its dysfunction has been implicated in the development and progression of neurodegenerative diseases.

TRBV6-7 is a small non-coding RNA molecule that consists of 23 amino acid residues. It is expressed in a variety of tissues throughout the body, including the brain, and is primarily localized to the cytoplasm of neurons. TRBV6-7 has been shown to play a role in the regulation of protein synthesis in the brain, and is required for the translation of several key proteins that are involved in brain function.

One of the most significant functions of TRBV6-7 is its role in the regulation of the translation of survival motor neuron (SMN) pre-mRNA. The SMN protein is a critical factor for the survival of motor neurons, and is abnormal expression in many A leading cause of neurodegenerative diseases, including Alzheimer's disease. TRBV6-7 can bind to the promoter region of SMN, thereby inhibiting its transcription and affecting its translation.

In addition, TRBV6-7 is also related to neuronal apoptosis. Studies have shown that neuronal apoptosis is regulated by multiple signaling pathways, including TRBV6-7. When neurons are damaged or die, TRBV6-7 can increase the incidence of apoptosis, thereby playing an important role in the development of neurodegenerative diseases.

Abnormal expression of TRBV6-7 has also been implicated in other neurodegenerative diseases, including Parkinson's disease and Huntington's disease. In addition, TRBV6-7 has been shown to play a role in the regulation of cellular processes such as cell adhesion, migration and invasion.

TRBV6-7 is also a potential drug target in the field of neurodegenerative diseases because of its role in the regulation of protein synthesis and its involvement in the regulation of cellular processes that are important for the development and progression of neurodegenerative diseases. The identification of TRBV6 -7 as a potential drug target has the potential to lead to new treatments for neurodegenerative diseases.

In conclusion, TRBV6-7 is a non-coding RNA molecule that has been identified as a potential drug target (also known as biomarker) in the field of neurodegenerative diseases. Its role in the regulation of protein synthesis and its involvement in the regulation of cellular processes that are important for the development and progression of neurodegenerative diseases make it an attractive target for drug development. Further research is needed to fully understand the function of TRBV6-7 and its potential as a drug target in the treatment of neurodegenerative diseases.

Protein Name: T Cell Receptor Beta Variable 6-7 (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 "TRBV6-7 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 TRBV6-7 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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