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The GNMT N-Terminal Domain Orchestrates Folate-Dependent Regulation of Cellular Methylation Dynamics
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Structural highlights
DiseaseGNMT_HUMAN Defects in GNMT are the cause of glycine N-methyltransferase deficiency (GNMT deficiency) [MIM:606664; also known as hypermethioninemia. The only clinical abnormalities in patients with this deficiency are mild hepatomegaly and chronic elevation of serum transaminases. FunctionGNMT_HUMAN Catalyzes the methylation of glycine by using S-adenosylmethionine (AdoMet) to form N-methylglycine (sarcosine) with the concomitant production of S-adenosylhomocysteine (AdoHcy). Possible crucial role in the regulation of tissue concentration of AdoMet and of metabolism of methionine.[1] [2] References
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This page was last modified 07:02, 17 June 2026.