Literature summary for 2.1.1.17 extracted from

Jacobs, R.L.; Jiang, H.; Kennelly, J.P.; Orlicky, D.J.; Allen, R.H.; Stabler, S.P.; Maclean, K.N.
Cystathionine beta-synthase deficiency alters hepatic phospholipid and choline metabolism Post-translational repression of phosphatidylethanolamine N-methyltransferase is a consequence rather than a cause of liver injury in homocystinuria (2017), Mol. Genet. Metab., 120, 325-336 .

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Organism

Organism	UniProt	Comment	Textmining
Mus musculus	Q61907	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
liver	-	Mus musculus	-

General Information

General Information	Comment	Organism
physiological function	a transgenic HO mouse model of classical homocystinuria exhibits only mild liver injury. Hepatic expression of PEMT in both the cystathionine beta-synthase-/- and HO models is post-translationally repressed with decreased levels of PEMT protein and activity that inversely correlates with the scale of liver injury. PEMT in HO mice is not further induced by increased homocysteine, methionine and S-adenosylhomocysteine or depletion of glutathione	Mus musculus

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Release 2023.1 (January 2023)