Target Name: AMT
NCBI ID: G275
Other Name(s): Aminomethyltransferase, mitochondrial (isoform 1) | nonketotic hyperglycinemia | GCST_HUMAN | GCE | Aminomethyltransferase, mitochondrial | Aminomethyltransferase (glycine cleavage system protein T) | aminomethyltransferase | AMT variant 1 | glycine cleavage system T protein | Glycine cleavage system T protein | GCST | NKH | Aminomethyltransferase, transcript variant 1 | GCVT

AMT: A promising drug target for the treatment of mitochondrial disease

Mitochondrial dysfunction (MND) is a condition characterized by a range of disorders that affect the function of mitochondria, leading to a variety of symptoms and diseases. One of the leading causes of MND is Aminomethyltransferase (AMT), a gene mutation that results in the production of a non-functional enzyme. In this article, we will discuss AMT and its potential as a drug target for the treatment of mitochondrial disease.

AMT: The foundation of mitochondrial disease

AMT is a gene that encodes the enzyme aminomethyltransferase (AMT). The AMT enzyme plays a crucial role in the regulation of DNA methylation, which is the process by which the cell protects its genetic material from being damaged or expressed. Methylation is a critical process that helps maintain the integrity of the genome and ensures the transmission of genetic information from one generation to the next.

However, in individuals with AMT mutations, the enzyme does not function properly, leading to a build-up of unmethylated DNA in the mitochondria. This accumulation of unmethylated DNA is associated with a range of symptoms and diseases, including MND, Alzheimer's, and cancer.

The impact of AMT mutations on human health

AMT mutations have been linked to a number of MND-related diseases, including:

1. Alzheimer's disease: Alzheimer's disease is a degenerative brain disorder that is characterized by the accumulation of neurofibrillary tangles and beta-amyloid plaques. The presence of these tangles and plaques is thought to be caused by the build-up of unmethylated DNA in the brain, which is thought to contribute to the misfolding of proteins and the formation of aggregates that are toxic to nerve cells.
2. Parkinson's disease: Parkinson's disease is a neurodegenerative disorder that is characterized by the loss of dopamine-producing neurons in the brain. The build-up of unmethylated DNA in the brain is thought to contribute to the misfolding of dopamine-producing proteins and the formation of aggregates that are toxic to the neurons.
3. Dot-rich repeat-containing neurodegenerative diseases (DRNDs): DRNDs are a group of inherited neurodegenerative diseases that are characterized by the accumulation of dot-rich repeat mutations in the brain. The build-up of unmethylated DNA in the brain is thought to contribute to the misfolding of proteins and the formation of aggregates that are toxic to the neurons.

AMT as a drug target

AMT has been identified as a potential drug target for the treatment of MND due to its role in the regulation of DNA methylation. By inhibiting the activity of AMT, researchers have found that they can reduce the build-up of unmethylated DNA in the mitochondria, which can lead to the reversal of MND-related symptoms.

One of the compounds that has been shown to inhibit the activity of AMT is called 5-methyl-3-phenyl-1-propanethiol (5-MPG). 5-MPG is a natural compound that has been found to be a potent inhibitor of AMT, and has been shown to improve cognitive function and reduce the build-up of unmethylated DNA in the brain.

Another compound that has been shown to inhibit AMT is called 2-methylphenyl-4-pyrimidone (2-MPP). 2-MP

Protein Name: Aminomethyltransferase

Functions: The glycine cleavage system catalyzes the degradation of glycine

More Common Targets

AMTN | AMY1A | AMY1B | AMY1C | AMY2A | AMY2B | Amylin receptor | Amyloid beta A4 precursor protein-binding family (APP-BP) | AMZ1 | AMZ2 | AMZ2P1 | Anandamide membrane transporter (AMT) | ANAPC1 | ANAPC10 | ANAPC10P1 | ANAPC11 | ANAPC13 | ANAPC15 | ANAPC16 | ANAPC1P1 | ANAPC1P2 | ANAPC2 | ANAPC4 | ANAPC5 | ANAPC7 | ANG | ANGEL1 | ANGEL2 | Angiogenic Factor | Angiotensin receptor (AT) | ANGPT1 | ANGPT2 | ANGPT4 | ANGPTL1 | ANGPTL2 | ANGPTL3 | ANGPTL4 | ANGPTL5 | ANGPTL6 | ANGPTL7 | ANGPTL8 | ANHX | ANK1 | ANK2 | ANK3 | ANKAR | ANKDD1A | ANKDD1B | ANKEF1 | ANKFN1 | ANKFY1 | ANKH | ANKHD1 | ANKHD1-EIF4EBP3 | ANKIB1 | ANKK1 | ANKLE1 | ANKLE2 | ANKMY1 | ANKMY2 | ANKRA2 | ANKRD1 | ANKRD10 | ANKRD11 | ANKRD12 | ANKRD13A | ANKRD13B | ANKRD13C | ANKRD13D | ANKRD16 | ANKRD17 | ANKRD18A | ANKRD18B | ANKRD18CP | ANKRD18DP | ANKRD19P | ANKRD2 | ANKRD20A1 | ANKRD20A11P | ANKRD20A12P | ANKRD20A13P | ANKRD20A17P | ANKRD20A18P | ANKRD20A19P | ANKRD20A2P | ANKRD20A3P | ANKRD20A4-ANKRD20A20P | ANKRD20A4P | ANKRD20A5P | ANKRD20A8P | ANKRD20A9P | ANKRD22 | ANKRD23 | ANKRD24 | ANKRD26 | ANKRD26P1 | ANKRD26P3 | ANKRD27 | ANKRD28 | ANKRD29