NALCN: A Potential Drug Target for Energy Metabolism and Disease

Target Name: NALCN

NCBI ID: G259232

NALCN

NALCN: A Potential Drug Target for Energy Metabolism and Disease

NALCN (N-acetyl-L-citrate synthase) is a protein that is expressed in various tissues throughout the body. It is a key enzyme in the citric acid cycle, also known as the Krebs cycle or tricarboxylic acid (TCA) cycle, which is a central metabolic pathway that generates energy in the form of ATP. The NALCN protein is a key player in this pathway, as it catalyzes the conversion of acetyl-CoA to malate and CoA, which are crucial intermediates in the TCA cycle.

Recent studies have identified NALCN as a potential drug target for various diseases, including cancer, neurodegenerative diseases, and cardiovascular diseases. The potential mechanisms by which NALCN may be targeted include its role in cellular signaling pathways, its involvement in energy metabolism, and its potential as a therapeutic target for diseases that involve the TCA cycle.

One of the potential mechanisms by which NALCN may be targeted is its role in cellular signaling pathways. NALCN is a key regulator of the TCA cycle, and its activity has been shown to be involved in a variety of cellular signaling pathways. For example, NALCN has been shown to be involved in the regulation of cell growth, differentiation, and apoptosis, as well as in the regulation of cell signaling pathways such as cell proliferation and survival.

In addition to its role in cellular signaling pathways, NALCN is also involved in energy metabolism. As a key player in the TCA cycle, NALCN is involved in the conversion of acetyl-CoA to malate and CoA, which are crucial intermediates in the production of ATP energy. This activity makes NALCN a critical component of the cell's energy metabolic pathway, and its dysfunction has been implicated in a variety of neurodegenerative diseases.

Another potential mechanism by which NALCN may be targeted is its potential as a therapeutic target for diseases that involve the TCA cycle. The TCA cycle is a central metabolic pathway that is involved in the production of ATP energy, and its dysfunction has been implicated in a variety of diseases, including cancer, neurodegenerative diseases, and cardiovascular diseases. By targeting NALCN, researchers may be able to disrupt its activity and reduce the production of ATP energy, which could have therapeutic benefits in these diseases.

In conclusion, NALCN is a protein that is expressed in various tissues throughout the body and is involved in the TCA cycle, which is a central metabolic pathway that generates energy in the form of ATP. Recent studies have identified NALCN as a potential drug target for various diseases, including cancer, neurodegenerative diseases, and cardiovascular diseases. Its potential mechanisms of action include its role in cellular signaling pathways, its involvement in energy metabolism, and its potential as a therapeutic target for diseases that involve the TCA cycle. Further research is needed to fully understand the potential therapeutic benefits of NALCN, and to develop safe and effective treatments for these diseases.

Protein Name: Sodium Leak Channel, Non-selective

Functions: Voltage-gated ion channel responsible for the resting Na(+) permeability that controls neuronal excitability (PubMed:17448995, PubMed:31409833). NALCN channel functions as a multi-protein complex, which consists at least of NALCN, NALF1, UNC79 and UNC80 (PubMed:32494638, PubMed:33203861). NALCN is the voltage-sensing, pore-forming subunit of the NALCN channel complex (PubMed:17448995). NALCN channel complex is constitutively active and conducts monovalent cations but is blocked by physiological concentrations of extracellular divalent cations (PubMed:32494638). In addition to its role in regulating neuronal excitability, is required for normal respiratory rhythm, systemic osmoregulation by controlling the serum sodium concentration and in the regulation of the intestinal pace-making activity in the interstitial cells of Cajal (By similarity). NALCN channel is also activated by neuropeptides such as neurotensin and substance P (SP) through a SRC family kinases-dependent pathway (By similarity). In addition, NALCN activity is enhanced/modulated by several GPCRs, such as CHRM3 (By similarity)

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•   general information;
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•   protein biological mechanisms;
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•   the target screening and validation;
•   expression level;
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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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