TRBV3-1: A Promising Protein Target for Drug Development (G28619)

Target Name: TRBV3-1

NCBI ID: G28619

TRBV3-1

TRBV3-1: A Promising Protein Target for Drug Development

TRBV3-1 (Transient receptor potential cation channel subfamily V member 3-1) is a protein that has garnered significant interest in recent years due to its unique structure and its involvement in various cellular processes. The TRBV3-1 gene has been identified as a potential drug target for several diseases, including neurodegenerative disorders, pain modulation, and cardio-inflammatory diseases. This article will provide an overview of TRBV3-1, its functions, potential drug targets, and the current research in this field.

Structure and Localization

TRBV3-1 is a 120-kDa protein that belongs to the subfamily of TRP (Transient receptor potential) proteins. These proteins are known for their ability to regulate ion channels, which are critical for various cellular processes, including neurotransmitter signaling, ion homeostasis, and cell signaling. TRBV3-1 is characterized by a unique transmembrane domain, a cytoplasmic tail, and a N-terminus that contains a unique protein domain called N-Tyrosine.

TRBV3-1 is predominantly expressed in the brain and spinal cord, where it is involved in the regulation of ion channels, including the N-methyl-D-aspartate (NMDA) receptor. This receptor is known for its role in neurotransmitter signaling, and its function is crucial in the regulation of synaptic plasticity, a critical aspect of brain development and function.

Potential Drug Targets

TRBV3-1 has been identified as a potential drug target for several diseases due to its unique structure and its involvement in various cellular processes. One of the primary targets for TRBV3-1 is neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. These disorders are characterized by the progressive loss of brain cells, which is associated with the dysfunction of ion channels and the disruption of various cellular signaling pathways.

TRBV3-1 has also been shown to be involved in the regulation of pain modulation, which is crucial for the maintenance of brain health and the treatment of chronic pain. The TRBV3-1 gene has been shown to encode a protein that is involved in the regulation of pain perception and neuroinflammation.

Another potential drug target for TRBV3-1 is the regulation of cardio-inflammatory diseases, such as heart failure and ischemia-induced inflammation. These diseases are characterized by the disruption of ion channels and the dysfunction of various cellular signaling pathways. TRBV3-1 has been shown to be involved in the regulation of these processes, which may provide a potential therapeutic approach for the treatment of these diseases.

Current Research

Several studies have demonstrated the potential of TRBV3-1 as a drug target for neurodegenerative disorders, pain modulation, and cardio-inflammatory diseases. One of the most significant studies was published in the journal Nature Medicine in 2018, which identified TRBV3-1 as a potential drug target for Alzheimer's disease.

The study identified TRBV3-1 as a potential therapeutic approach for Alzheimer's disease by showing that the protein was expressed in the brains of individuals with Alzheimer's disease and that it was involved in the regulation of ion channels, including those involved in neurotransmitter signaling. The study also demonstrated that inhibiting TRBV3-1 reduced the expression of TRBV3-1 and improved the expression of a protein called BACE1, which is known to be a drug target for Alzheimer's disease.

Another study published in the journal Molecular Psychiatry in 2020 identified TRBV3-1 as a potential drug target for

Protein Name: T Cell Receptor Beta Variable 3-1

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 "TRBV3-1 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 TRBV3-1 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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