[{"from": "human", "value": "Provide a description of this molecule. [C][=N][C][=Branch2][Ring2][=N][=C][C][=Branch1][Ring2][=N][Ring1][=Branch1][N][Branch1][Branch1][C][=N][Ring1][=Branch1][C@H1][C@@H1][Branch2][Ring1][=Branch2][C@@H1][Branch2][Ring1][Ring2][C@H1][Branch1][Ring2][O][Ring1][Branch1][C][S][C][C][C@@H1][Branch1][=Branch1][C][=Branch1][C][=O][O][N][O][O][N]"}, {"from": "gpt", "value": "The molecule is the immediate precursor of all of the homocysteine produced in the body. The reaction is catalyzed by S-adenosylhomocysteine hydrolase and is reversible with the equilibrium favoring formation of AdoHcy. In vivo, the reaction is driven in the direction of homocysteine formation by the action of the enzyme adenosine deaminase, which converts the second product of the S-adenosylhomocysteine hydrolase reaction, adenosine, to inosine. Except for methyl transfer from betaine and from methylcobalamin in the methionine synthase reaction, AdoHcy is the product of all methylation reactions that involve S-adenosylmethionine (AdoMet) as the methyl donor. Methylation is significant in epigenetic regulation of protein expression via DNA and histone methylation. The inhibition of these AdoMet-mediated processes by AdoHcy is a proven mechanism for metabolic alteration. Because the conversion of AdoHcy to homocysteine is reversible, with the equilibrium favoring the formation of AdoHcy, increases in plasma homocysteine are accompanied by an elevation of AdoHcy in most cases. Disturbances in the transmethylation pathway indicated by abnormal S-adenosylmethionine, S-adenosylhomocysteine or their ratio have been reported in many neurodegenerative diseases, such as dementia, depression or Parkinson's disease.  (A3511, A3512)."}]