4ign: Difference between revisions
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4ign FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4ign OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4ign RCSB], [http://www.ebi.ac.uk/pdbsum/4ign PDBsum]</span></td></tr> | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4ign FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4ign OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4ign RCSB], [http://www.ebi.ac.uk/pdbsum/4ign PDBsum]</span></td></tr> | ||
</table> | </table> | ||
== Function == | |||
[[http://www.uniprot.org/uniprot/ACMSD_HUMAN ACMSD_HUMAN]] Converts alpha-amino-beta-carboxymuconate-epsilon-semialdehyde (ACMS) to alpha-aminomuconate semialdehyde (AMS). ACMS can be converted non-enzymatically to quinolate (QA), a key precursor of NAD, and a potent endogenous excitotoxin of neuronal cells which is implicated in the pathogenesis of various neurodegenerative disorders. In the presence of ACMSD, ACMS is converted to AMS, a benign catabolite. ACMSD ultimately controls the metabolic fate of tryptophan catabolism along the kynurenine pathway.<ref>PMID:19843166</ref> <ref>PMID:12140278</ref> | |||
<div style="background-color:#fffaf0;"> | <div style="background-color:#fffaf0;"> | ||
== Publication Abstract from PubMed == | == Publication Abstract from PubMed == | ||
