Adenosylhomocysteinase (AHCY) is involved in the hydrolysis of adenosylselenohomocysteine (AdeSeHCys) into adenosine and selenohomocysteine (SeHCys). This reaction is inferred from the event in rat involving the protein adenosylhomocysteinase (Ahcy) (Kajander et al. 1991, Kajander and Raina 1981).
Adenosylhomocysteinase (AHCY) is a tetrameric, NAD+-bound, cytosolic protein that regulates all adenosylmethionine-(AdoMet) dependent transmethylations by hydrolysing the feedback inhibitor adenosylhomocysteine (AdoHcy) to homocysteine (HCYS) and adenosine (Ade-Rib) (Turner et al. 1998, Yang et al. 2003). Defects in AHCY cause Hypermethioninemia with S-adenosylhomocysteine hydrolase deficiency (HMAHCHD; MIM:613752), a metabolic disorder characterised by hypermethioninemia associated with failure to thrive, psychomotor retardation, facial dysmorphism with abnormal hair and teeth and myocardiopathy. Gene analysis revealed two mutations that can cause HMAHCHD; W112* and Y143C (Baric et al. 2004).
Adenosylhomocysteinase (AHCY) is a tetrameric, NAD+-bound, cytosolic protein that regulates all adenosylmethionine-(AdoMet) dependent transmethylations by hydrolysing the feedback inhibitor adenosylhomocysteine (AdoHcy) to homocysteine (HCYS) and adenosine (Ade-Rib) (Turner et al. 1998, Yang et al. 2003).
Putative adenosylhomocysteinase 2 (AHCYL1 aka adenosylhomocysteine hydrolase-like protein 1) (Dekker et al. 2002) possesses 50% homology to adenosylhomocysteine hydrolase (AHCY), an enzyme important for metabolizing S-adenosyl-l-homocysteine. AHCYL1 can bind to the inositol 1,4,5-trisphosphate receptor (ITPR1) tetramer, suggesting that AHCYL1 is involved in modulating intracellular calcium release (Cooper et al. 2006).