Glycine N-methyltransferase (GMNT) regulates the ratio of S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH) and has a role in methionine metabolism and methylation of DNA and histones. GNMT is down-regulated in patients with liver cirrhosis and/or hepatocellular carcinoma. 
These mice carry a targeted mutation of the Gnmt gene. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross behavioral abnormalities. No gene product (protein) is detected by Western blot or enzyme activity analysis of liver from homozygous mice. Homozygotes exhibit increased levels of free methionine and SAM (35 fold) in the liver, and decreased SAH levels in the liver, with the ratio of SAM/SAH elevated 100-fold. Serum levels of aminotransferases, methionine, and SAM are also elevated. Although heterozygotes have only approximately 50% of wildtype enzyme activity levels, hepatic methione, SAM and SAH levels are similar to wildtype control. At 3 months of age, homozygotes exhibit progressive liver steatosis and fibrosis. At 8 months of age, homozygotes exhibit hypermethlyation of DNA and develop multifocal hepatocellular carcinoma.

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In this strain a NEO cassette replaces exon1 and the promoter region of the Gnmt gene. This strain is a model for Glycine N-Methyltransferase Deficiency and has applications in studies of methionine metabolism, methylation and molecular markers for hepatocellular carcinoma.

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