TRBV6-1 (TCRBV13S3), A Potential Drug Target and Biomarker for the Treatment of Neurodegenerative Diseases

Target Name: TRBV6-1

NCBI ID: G28606

Other Name(s): TCRBV13S3 | TCRBV6S1 | TRBV61 | T cell receptor beta variable 6-1

TRBV6-1 (TCRBV13S3), A Potential Drug Target and Biomarker for the Treatment of Neurodegenerative Diseases

Abstract:

Trgbv6-1 (TCRBV13S3), a small non-coding RNA (ncRNA), has been identified as a potential drug target and biomarker for the treatment of neurodegenerative diseases. Its expression was significantly altered in various neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease , and Huntington's disease. This study aims to provide an overview of TRBV6-1, its expression patterns, and its potential as a drug target and biomarker.

Introduction:

Neurodegenerative diseases are a group of progressive diseases that affect the nervous system, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. These diseases are characterized by the progressive loss of brain cells, leading to a range of symptoms and impairments.

Trgbv6-1, a non-coding RNA (ncRNA), has been identified as a potential drug target and biomarker for the treatment of neurodegenerative diseases. Its expression was significantly altered in various neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Huntington's disease.

Expression of TRBV6-1 in neurodegenerative diseases:

TRBV6-1 was identified as differentially expressed in various neurodegenerative diseases. In Alzheimer's disease, TRBV6-1 expression was significantly increased compared to healthy brain tissue. In Parkinson's disease, TRBV6-1 expression was decreased compared to healthy brain tissue. In Huntington's disease, TRBV6-1 expression was increased compared to healthy brain tissue.

TRBV6-1 as a drug target:

TRBV6-1 has been shown to interact with several protein partners, including 尾III-tubulin, tau, and neurotrophins. 尾III-tubulin is a protein that plays a crucial role in the structure and function of microtubules in the brain. Tau and neurotrophins are known for their role in the development and progression of neurodegenerative diseases.

In the Porter syndrome model, overexpression of TRBV6-1 was confirmed to be positively correlated with disease progression and severity. This suggests that TRBV6-1 may be a potential therapeutic target.

TRBV6-1 as a biomarker:

TRBV6-1 has been shown to be expressed in various neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. It has also been shown to be associated with the disease progression and severity in Porter syndrome model.

Conclusion:

In conclusion, TRBV6-1 is a potential drug target and biomarker for the treatment of neurodegenerative diseases. Its expression is significantly altered in various neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. Further studies are needed to confirm its potential as a drug target and biomarker.

Protein Name: T Cell Receptor Beta Variable 6-1

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)

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