4o1l: Difference between revisions
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==Human Adenosine Kinase in complex with inhibitor== | |||
<StructureSection load='4o1l' size='340' side='right'caption='[[4o1l]], [[Resolution|resolution]] 2.50Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[4o1l]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4O1L OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4O1L FirstGlance]. <br> | |||
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.5Å</td></tr> | |||
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=HO4:5-ETHYNYL-7-(BETA-D-RIBOFURANOSYL)-7H-PYRROLO[2,3-D]PYRIMIDIN-4-AMINE'>HO4</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr> | |||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=4o1l FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4o1l OCA], [https://pdbe.org/4o1l PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4o1l RCSB], [https://www.ebi.ac.uk/pdbsum/4o1l PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4o1l ProSAT]</span></td></tr> | |||
</table> | |||
== Disease == | |||
[https://www.uniprot.org/uniprot/ADK_HUMAN ADK_HUMAN] Defects in ADK are the cause of hypermethioninemia due to adenosine kinase deficiency (HMAKD) [MIM:[https://omim.org/entry/614300 614300]. A metabolic disorder characterized by global developmental delay, early-onset seizures, mild dysmorphic features, and characteristic biochemical anomalies, including persistent hypermethioninemia with increased levels of S-adenosylmethionine and S-adenosylhomocysteine. Homocysteine levels are typically normal.<ref>PMID:21963049</ref> | |||
== Function == | |||
[https://www.uniprot.org/uniprot/ADK_HUMAN ADK_HUMAN] ATP dependent phosphorylation of adenosine and other related nucleoside analogs to monophosphate derivatives. Serves as a potential regulator of concentrations of extracellular adenosine and intracellular adenine nucleotides. | |||
==See Also== | |||
*[[Adenosine kinase 3D structures|Adenosine kinase 3D structures]] | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Homo sapiens]] | |||
[[Category: Large Structures]] | |||
[[Category: Brynda J]] | |||
[[Category: Dostal J]] | |||
[[Category: Hodcek M]] | |||
[[Category: Pichova I]] | |||
Latest revision as of 11:57, 20 March 2024
Human Adenosine Kinase in complex with inhibitorHuman Adenosine Kinase in complex with inhibitor
Structural highlights
DiseaseADK_HUMAN Defects in ADK are the cause of hypermethioninemia due to adenosine kinase deficiency (HMAKD) [MIM:614300. A metabolic disorder characterized by global developmental delay, early-onset seizures, mild dysmorphic features, and characteristic biochemical anomalies, including persistent hypermethioninemia with increased levels of S-adenosylmethionine and S-adenosylhomocysteine. Homocysteine levels are typically normal.[1] FunctionADK_HUMAN ATP dependent phosphorylation of adenosine and other related nucleoside analogs to monophosphate derivatives. Serves as a potential regulator of concentrations of extracellular adenosine and intracellular adenine nucleotides. See AlsoReferences
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