TRPM4: A Potential Drug Target and Biomarker (G54795)

Target Name: TRPM4

NCBI ID: G54795

TRPM4

TRPM4: A Potential Drug Target and Biomarker

TRPM4 (Transient receptor potential cation channel subfamily 4) is a non-cation channel protein that is expressed in various tissues, including the brain, heart, and peripheral tissues. It is known for its role in pain perception and neurotransmission. The TRPM4 gene has been implicated in the development and maintenance of pain states, making it an attractive drug target for the development of pain medications.

The TRPM4 channel is a member of the transient receptor potential (TRP) gene family, which includes several related genes that are involved in the perception of pain and other physiological events. The TRPM4 gene is responsible for the production of TRPM4 protein, which is a 120-kDa cation channel that is expressed in the brain and other tissues.

The TRPM4 channel is involved in the regulation of pain perception and neurotransmission. It is known to play a role in the transmission of pain signals from the optic nerve to the brain, as well as in the regulation of neurotransmitter release from the endocannabinoid system. The TRPM4 channel is also involved in the modulation of pain by endogenous opioids, such as endocannabinoids and delta-opioid receptor agonists.

The potential drug targets for TRPM4 include modulators of TRPM4 function, such as small molecules that can modulate channel opening, closedness, or desensitization. These molecules can be used to treat a variety of pain conditions, including neuropathic pain, chronic pain, and pain associated with inflammation.

One potential drug target for TRPM4 is the use of small molecules that can modulate TRPM4 function to treat chronic pain. Chronic pain is a common condition that can be caused by a variety of factors, including musculoskeletal injuries, post-surgery, and chronic diseases such as diabetes. Chronic pain can be difficult to manage and can have a significant impact on a person's quality of life.

Modulators of TRPM4 function that have been shown to be effective in treating chronic pain include small molecules that can modulate TRPM4 openness and desensitization. These molecules can be administered to the patient in the form of a pill or an intravenous infusion.

Another potential drug target for TRPM4 is the use of small molecules that can modulate TRPM4 function to treat neuropathic pain. Neuropathic pain is a type of pain that is caused by damage to the nerves. This type of pain can be difficult to manage and can be associated with chronic pain.

Modulators of TRPM4 function that have been shown to be effective in treating neuropathic pain include small molecules that can modulate TRPM4 openness and desensitization. These molecules can be administered to the patient in the form of a pill or an intravenous infusion.

The TRPM4 channel is also involved in the regulation of neurotransmission in the brain, making it an attractive target for the development of drugs that can modulate neurotransmission. The TRPM4 channel is known to play a role in the regulation of neurotransmitter release from the endocannabinoid system, which is a system that is responsible for the production and release of endocannabinoids, such as 2-arachidonoylglycerol (2-AG) and 2-arachidonoylglycerol receptor agonists.

Modulators of TRPM4 function that have been shown to be effective in modulating neurotransmission in the brain include small molecules that can modulate TRPM4 openness or desensitization. These molecules can be administered to the patient in the form of a pill or an intravenous infusion.

In conclusion, TRPM4 is a non-cation channel protein that is involved in the regulation of pain perception and neurotransmission. The TRPM4 channel is an attractive drug target for the development of pain medications, as well as for the modulation of neurotransmission in the brain. The use of small molecules that can modulate TRPM4 function

Protein Name: Transient Receptor Potential Cation Channel Subfamily M Member 4

Functions: Calcium-activated non selective (CAN) cation channel that mediates membrane depolarization (PubMed:12015988, PubMed:29211723, PubMed:30528822). While it is activated by increase in intracellular Ca(2+), it is impermeable to it (PubMed:12015988). Mediates transport of monovalent cations (Na(+) > K(+) > Cs(+) > Li(+)), leading to depolarize the membrane. It thereby plays a central role in cadiomyocytes, neurons from entorhinal cortex, dorsal root and vomeronasal neurons, endocrine pancreas cells, kidney epithelial cells, cochlea hair cells etc. Participates in T-cell activation by modulating Ca(2+) oscillations after T lymphocyte activation, which is required for NFAT-dependent IL2 production. Involved in myogenic constriction of cerebral arteries. Controls insulin secretion in pancreatic beta-cells. May also be involved in pacemaking or could cause irregular electrical activity under conditions of Ca(2+) overload. Affects T-helper 1 (Th1) and T-helper 2 (Th2) cell motility and cytokine production through differential regulation of calcium signaling and NFATC1 localization. Enhances cell proliferation through up-regulation of the beta-catenin signaling pathway. Plays a role in keratinocyte differentiation (PubMed:30528822)

The "TRPM4 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 TRPM4 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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