CRTAM: A Potential Drug Target and Biomarker for T Cell-Related Diseases

Target Name: CRTAM

NCBI ID: G56253

CRTAM

CRTAM: A Potential Drug Target and Biomarker for T Cell-Related Diseases

Abstract:

Chlorpromazine (CRTAM) is a N-methyl-D-aspartate (NMDA) receptor antagonist that has been shown to have therapeutic potential in various neurodegenerative diseases, including Alzheimer's disease. However, its underlying mechanism of action is not fully understood. In this article, we will discuss the potential drug target and biomarker properties of CRTAM, as well as its current status as a drug development target.

Introduction:

T cells play a crucial role in the immune system and are involved in a wide range of physiological processes, including fighting off infections and neutralizing foreign antigens. T cells are also involved in the development and maintenance of the nervous system, and are thought to contribute to the development and progression of neurodegenerative diseases.

One of the molecules that have been implicated in T cell-related diseases is the chlorpromazine (CRTAM) receptor. CRTAM is a N-methyl-D-aspartate (NMDA) receptor antagonist that has been shown to have therapeutic potential in various neurodegenerative diseases, including Alzheimer's disease.

Drug Target and Biomarker Properties of CRTAM:

The CRTAM receptor is a potential drug target for T cell-related diseases because it has been shown to play a role in the development and progression of these diseases. Studies have shown that CRTAM antagonists can improve cognitive function in models of neurodegenerative diseases, including Alzheimer's disease.

In addition to its potential therapeutic uses, CRTAM has also been shown to be a potential biomarker for the diagnosis and monitoring of neurodegenerative diseases. Its loss has been observed in various neurodegenerative diseases, including Alzheimer's disease, and its levels have been used as a biomarker to track the progression of these diseases.

Current Status of CRTAM as a Drug Development Target:

CRTAM is currently being targeted as a potential drug development target for T cell-related diseases. Several studies have shown that CRTAM antagonists have the potential to treat a wide range of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and multiple sclerosis.

One of the main advantages of CRTAM as a drug development target is its ability to cross the blood-brain barrier and its potential to target the NMDA receptor in T cells. This allows for its potential to have a more potent and long-lasting effect on T cells and their associated diseases.

CRTAM-Induced T Cell Activation:

Studies have shown that CRTAM has the ability to induce T cell activation and activation-induced cell death (AICD) in a dose-dependent manner. This is thought to be due to the fact that CRTAM blocks the inhibition of intracellular signaling pathways that are involved in T cell activation and cell death.

In addition to its ability to induce T cell activation, CRTAM has also been shown to have the ability to modulate the expression of genes involved in T cell function and regulation. This includes the modulation of the expression of genes involved in the development and maintenance of T cells, as well as their role in immune surveillance.

CRTAM's Interaction with Other molecules:

Several studies have shown that CRTAM interacts with several other molecules involved in the development and progression of T cell-related diseases. These include molecules involved in intracellular signaling pathways, such as the T cell receptor (TCR), and molecules involved in cell death and survival, such as Bcl-2 and p53.

In addition to its interaction with these molecules, CRTAM has also been shown to interact with molecules involved in the regulation of inflammation and immune surveillance, including NF-kappa-B and

Protein Name: Cytotoxic And Regulatory T Cell Molecule

Functions: Mediates heterophilic cell-cell adhesion which regulates the activation, differentiation and tissue retention of various T-cell subsets (By similarity). Interaction with CADM1 promotes natural killer (NK) cell cytotoxicity and IFNG/interferon-gamma secretion by CD8+ T-cells in vitro as well as NK cell-mediated rejection of tumors expressing CADM1 in vivo (PubMed:15811952). Regulates CD8+ T-cell proliferation in response to T-cell receptor (TCR) activation (By similarity). Appears to be dispensable for CD8+ T-cell-mediated cytotoxicity (By similarity). Interaction with SCRIB promotes the late phase of cellular polarization of a subset of CD4+ T-cells, which in turn regulates TCR-mediated proliferation and IFNG, IL17 and IL22 production (By similarity). By interacting with CADM1 on CD8+ dendritic cells, regulates the retention of activated CD8+ T-cells within the draining lymph node (By similarity). Required for the intestinal retention of intraepithelial CD4+ CD8+ T-cells and, to a lesser extent, intraepithelial and lamina propria CD8+ T-cells and CD4+ T-cells (By similarity). Interaction with CADM1 promotes the adhesion to gut-associated CD103+ dendritic cells, which may facilitate the expression of gut-homing and adhesion molecules on T-cells and the conversion of CD4+ T-cells into CD4+ CD8+ T-cells (By similarity)

The "CRTAM 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 CRTAM 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

More Common Targets