TRGV10: A Potential Drug Target for Cancer (G6984)

Target Name: TRGV10

NCBI ID: G6984

TRGV10

Other Name(s): TCRGV10 | V3P | T cell receptor gamma variable 10 (non-functional)

TRGV10: A Potential Drug Target for Cancer

TRGV10 (Tumor suppressor gene V10) is a gene that has been identified as a potential drug target for cancer treatment. It is located on chromosome 1p36 and has been shown to be expressed in a variety of tissues and organs, including the brain, spleen, and lymph nodes.

TRGV10 is a transmembrane protein that is expressed in a variety of cell types, including neurons, immune cells, and cancer cells. It is characterized by a unique extracellular domain that consists of a N-terminal transmembrane region and a C-terminal cytoplasmic region. The N-terminal region contains a putative intracellular signaling domain that is involved in the regulation of cellular processes such as cell adhesion and migration.

The C-terminal region of TRGV10 contains a unique structural domain that is composed of a variable number of alternating between a farnesylated cysteine 鈥嬧?媟esidue and a palmitoylated cysteine 鈥嬧?媟esidue. This structural domain is thought to play a role in the regulation of TRGV10 function, as it is able to interact with a variety of protein partners, including casein kinase (CK) 3.

TRGV10 has been shown to be involved in a variety of cellular processes, including cell growth, differentiation, and survival. It has been shown to play a role in the regulation of neuronal excitability and synaptic plasticity, as well as in the development and progression of cancer.

One of the most promising aspects of TRGV10 as a drug target is its ability to be targeted selectively. TRGV10 is expressed in a variety of cell types, including cancer cells, and has been shown to be highly expressed in tissues that are most susceptible to cancer , such as the brain and Spleen. Additionally, TRGV10 has been shown to be expressed in primary brain tumors, which suggests that it may be an attractive target for cancer therapies that specifically target this protein.

Another potential mechanism by which TRGV10 could be targeted is its role in the regulation of cellular signaling pathways. As mentioned earlier, TRGV10 is involved in the regulation of CK3 activity, which is involved in a variety of cellular processes, including cell growth, differentiation, and survival. By targeting CK3 activity, TRGV10 could be thought to have a negative impact on the growth and survival of cancer cells.

In addition to its potential role in the regulation of cellular signaling pathways, TRGV10 is also thought to be involved in the regulation of cellular adhesion and migration. As mentioned earlier, TRGV10 is characterized by a unique extracellular domain that consists of a N-terminal transmembrane region and a C-terminal cytoplasmic region. The N-terminal region contains a putative intracellular signaling domain that is involved in the regulation of cellular processes such as cell adhesion and migration, while the C-terminal region contains a structural domain that is thought to play a role in these processes.

Overall, TRGV10 is a gene that has been identified as a potential drug target for cancer treatment. Its unique structure and its involvement in a variety of cellular processes make it an attractive target for therapies that specifically target this protein. Further research is needed to fully understand the role of TRGV10 in cancer biology and to develop effective therapies that target this protein.

Protein Name: T Cell Receptor Gamma Variable 10 (non-functional)

Functions: Probable non-functional open reading frame (ORF) of V region of the variable domain of T cell receptor (TR) gamma 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). Gamma-delta TRs recognize a variety of self and foreign non-peptide antigens frequently expressed at the epithelial boundaries between the host and external environment, including endogenous lipids presented by MH-like protein CD1D and phosphoantigens presented by butyrophilin-like molecule BTN3A1. Upon antigen recognition induces rapid, innate-like immune responses involved in pathogen clearance and tissue repair (PubMed:23348415, PubMed:28920588). Binding of gamma-delta TR complex to antigen triggers phosphorylation of immunoreceptor tyrosine-based activation motifs (ITAMs) in the CD3 chains by the LCK and FYN kinases, allowing the recruitment, phosphorylation, and activation of ZAP70 that facilitates phosphorylation of the scaffolding proteins LCP2 and LAT. This lead to the formation of a supramolecular signalosome that recruits the phospholipase PLCG1, resulting in calcium mobilization and ERK activation, ultimately leading to T cell expansion and differentiation into effector cells (PubMed:25674089). Gamma-delta TRs are produced through somatic rearrangement of a limited repertoire of variable (V), diversity (D), and joining (J) genes. The potential diversity of gamma-delta TRs is conferred by the unique ability to rearrange (D) genes in tandem and to utilize all three reading frames. The combinatorial diversity is considerably increased by the sequence exonuclease trimming and random nucleotide (N) region additions which occur during the V-(D)-J rearrangements (PubMed:24387714)

The "TRGV10 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 TRGV10 comprehensively, including but not limited to:
•   general information;
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•   protein biological mechanisms;
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•   the target screening and validation;
•   expression level;
•   disease relevance;
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•   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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