TRBV10-2: A Non-Code RNA Molecule as A Potential Drug Target for Neurodegenerative Diseases

Target Name: TRBV10-2

NCBI ID: G28584

TRBV10-2

Other Name(s): TCRBV12S3 | T cell receptor beta variable 10-2 | TRBV102 | TCRBV10S2

TRBV10-2: A Non-Code RNA Molecule as A Potential Drug Target for Neurodegenerative Diseases

TRBV10-2 (TcRBV12S3) 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, particularly in the context of Alzheimer's disease. The TRBV10-2 molecule is a key regulator of the translation of mRNAs in the brain, and its levels have been implicated in the progression of neurodegenerative diseases.

TRBV10-2 is a small non-coding RNA molecule that consists of 19 amino acid residues. It is expressed in a variety of tissues, including brain, heart, and testes, and has been identified as a potential drug target in the context of neurodegenerative diseases.

One of the key functions of TRBV10-2 is as a regulator of the translation of mRNAs in the brain. During translation, TRBV10-2 helps to ensure that the correct version of the gene's code is produced and that it is properly translated into the protein that is responsible for the neuronal function.

Research has suggested that disruptions in the translation of mRNAs, such as those caused by TRBV10-2, may contribute to the development and progression of neurodegenerative diseases. The levels of TRBV10-2 have been implicated in the progression of Alzheimer's disease, a neurodegenerative disease that is characterized by the progressive loss of brain cells and the development of neurofibrillary tangles and senescent bodies.

Another function of TRBV10-2 is its role as a negative regulator of the microRNA (miRNA) pathway. miRNA is a small non-coding RNA molecule that plays a critical role in regulating gene expression in the cell. TRBV10-2 has been shown to interact with miRNA-21, ami1241, and miRNA-181, a miRNA that is involved in the regulation of neuronal differentiation and the maintenance of brain cell stem cells.

The miRNA pathway is a complex process that involves the production, processing, and translation of miRNA molecules, as well as their interactions with target genes. TRBV10-2 has been shown to play a role in the regulation of miRNA expression by binding to the miRNA-21 complex and interacting with ami1241, a miRNA that is known to interact with TRBV10-2.

In addition to its role as a negative regulator of the miRNA pathway, TRBV10-2 has also been shown to play a role in the regulation of cellular processes that are important for brain development and function. For example, TRBV10-2 has been shown to be involved in the regulation of the formation of neuronal synapses, the process by which brain cells communicate with one another.

TRBV10-2 has also been shown to play a role in the regulation of cellular processes that are important for the maintenance of brain cells and the development of neurodegenerative diseases. For example, TRBV10-2 has been shown to be involved in the regulation of the apoptosis, or programmed cell death, of brain cells, a process that is important for the development of neurofibrillary tangles and other hallmarks of neurodegenerative diseases.

In conclusion, TRBV10-2 is a non-coding RNA molecule that has been identified as a potential drug target in the field of neurodegenerative diseases, particularly in the context of Alzheimer's disease. Its functions as a regulator of the translation of mRNAs and as a negative regulator of the miRNA pathway suggest that it may be a useful target for the development of new therapies for

Protein Name: T Cell Receptor Beta Variable 10-2

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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