6nn4: Difference between revisions
Jump to navigation
Jump to search
m Protected "6nn4" [edit=sysop:move=sysop] |
No edit summary |
||
| Line 1: | Line 1: | ||
The | ==The structure of human liver pyruvate kinase, hLPYK-D499N, in complex with Fru-1,6-BP== | ||
<StructureSection load='6nn4' size='340' side='right'caption='[[6nn4]], [[Resolution|resolution]] 2.15Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[6nn4]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6NN4 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6NN4 FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=FBP:BETA-FRUCTOSE-1,6-DIPHOSPHATE'>FBP</scene>, <scene name='pdbligand=PEP:PHOSPHOENOLPYRUVATE'>PEP</scene></td></tr> | |||
[[Category: | <tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Pyruvate_kinase Pyruvate kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.40 2.7.1.40] </span></td></tr> | ||
[[Category: Fenton, A | <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=6nn4 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6nn4 OCA], [http://pdbe.org/6nn4 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6nn4 RCSB], [http://www.ebi.ac.uk/pdbsum/6nn4 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6nn4 ProSAT]</span></td></tr> | ||
[[Category: | </table> | ||
[[Category: | == Disease == | ||
[[Category: Meneely, K | [[http://www.uniprot.org/uniprot/KPYR_HUMAN KPYR_HUMAN]] Defects in PKLR are the cause of pyruvate kinase hyperactivity (PKHYP) [MIM:[http://omim.org/entry/102900 102900]]; also known as high red cell ATP syndrome. This autosomal dominant phenotype is characterized by increase of red blood cell ATP.<ref>PMID:9090535</ref> Defects in PKLR are the cause of pyruvate kinase deficiency of red cells (PKRD) [MIM:[http://omim.org/entry/266200 266200]]. A frequent cause of hereditary non-spherocytic hemolytic anemia. Clinically, pyruvate kinase-deficient patients suffer from a highly variable degree of chronic hemolysis, ranging from severe neonatal jaundice and fatal anemia at birth, severe transfusion-dependent chronic hemolysis, moderate hemolysis with exacerbation during infection, to a fully compensated hemolysis without apparent anemia. | ||
[[Category: | == Function == | ||
[[http://www.uniprot.org/uniprot/KPYR_HUMAN KPYR_HUMAN]] Plays a key role in glycolysis (By similarity). | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Large Structures]] | |||
[[Category: Pyruvate kinase]] | |||
[[Category: Fenton, A W]] | |||
[[Category: Lamb, A L]] | |||
[[Category: McFarlane, J S]] | |||
[[Category: Meneely, K M]] | |||
[[Category: Ronnebaum, T A]] | |||
[[Category: Allosteric]] | |||
[[Category: Glycolysis]] | |||
[[Category: Transferase]] | |||