Genes involved in the methylation cycle
MTHFR
The MTHFR gene produces the enzyme methylenetetrahydrofolate reductase. It converts folate into its active form. This is crucial for converting the harmful amino acid homocysteine into methionine, which is safe for the body. Two common variants in this gene are C677T and A1298C, which can lead to overactivity of the MTHFR enzyme and increased homocysteine levels.
The MTRR gene produces the enzyme methionine synthase reductase. It plays a role in activating another enzyme, methionine synthase (MTR). The MTR enzyme directly converts homocysteine to methionine. Variants in the MTRR gene can result in impaired reactivation of MTR, leading to a buildup of homocysteine and reduced methionine levels.
The MTR gene produces the enzyme methionine synthase. This enzyme is responsible for the final step in the conversion of the amino acid homocysteine to methionine. Variants in the MTR gene can result in a buildup of homocysteine in the blood and decreased availability of methionine and SAM, which can disrupt DNA methylation and gene expression.
The CBS gene produces the enzyme cystathionine beta-synthase. It is crucial in the transsulfuration pathway, a branch of the methylation cycle. The CBS enzyme catalyzes the first step in the conversion of homocysteine to another amino acid called cysteine. Variants in the CBS gene can impair this conversion, leading to increased homocysteine levels.
The CPS1 gene produces the enzyme carbomyl phosphate synthetase. It plays an important role in the urea cycle, which converts excess ammonia in the body to urea. This cycle regulates neuronal health and oxidative stress. Variants in the CPS1 gene have been associated with higher homocysteine levels. However, the mechanism behind this is unclear.
The BHMT gene produces the enzyme betaine-homocysteine S-methyltransferase. It transfers a methyl group from a compound called betaine to homocysteine to convert it to methionine. Methionine is then converted to SAMe. Variants in the BHMT gene may affect the levels or activity of the enzyme and may result in higher homocysteine levels.
The SUOX gene catalyzes the oxidation of sulfite to sulfate, the final molybdenum-dependent reaction in the oxidative degradation of the sulfur amino acids cysteine and methionine. This gene product helps detoxify sulfites in the body. Variants in SUOX may result in sulfite sensitivity and neurological abnormalities, and should be considered in combination with upregulated CBS.
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