7frx: Difference between revisions

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-'''Unreleased structure'''
-The entry 7frx is ON HOLD
+==Structure of liver pyruvate kinase in complex with allosteric modulator 5==
+<StructureSection load='7frx' size='340' side='right'caption='[[7frx]], [[Resolution|resolution]] 1.85&Aring;' scene=''>
-Authors: Lulla, A., Nilsson, O., Brear, P., Nain-Perez, A., Grotli, M., Hyvonen, M.
+== Structural highlights ==
+<table><tr><td colspan='2'>[[7frx]] is a 8 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=7FRX OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7FRX FirstGlance]. <br>
-Description: Structure of liver pyruvate kinase in complex with allosteric modulator 5
+</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=FBP:BETA-FRUCTOSE-1,6-DIPHOSPHATE'>FBP</scene>, <scene name='pdbligand=K:POTASSIUM+ION'>K</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=O88:N-{[4-(3,4-dihydroxybenzene-1-sulfonyl)phenyl]methyl}-3,4-dihydroxybenzene-1-sulfonamide'>O88</scene>, <scene name='pdbligand=OXL:OXALATE+ION'>OXL</scene></td></tr>
-[[Category: Unreleased Structures]]
+<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7frx FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7frx OCA], [https://pdbe.org/7frx PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7frx RCSB], [https://www.ebi.ac.uk/pdbsum/7frx PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7frx ProSAT]</span></td></tr>
-[[Category: Brear, P]]
+</table>
-[[Category: Hyvonen, M]]
+== Disease ==
-[[Category: Nilsson, O]]
+[https://www.uniprot.org/uniprot/KPYR_HUMAN KPYR_HUMAN] Defects in PKLR are the cause of pyruvate kinase hyperactivity (PKHYP) [MIM:[https://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:[https://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: Lulla, A]]
+== Function ==
-[[Category: Grotli, M]]
+[https://www.uniprot.org/uniprot/KPYR_HUMAN KPYR_HUMAN] Plays a key role in glycolysis (By similarity).
-[[Category: Nain-Perez, A]]
+== References ==
+<references/>
+__TOC__
+</StructureSection>
+[[Category: Homo sapiens]]
+[[Category: Large Structures]]
+[[Category: Brear P]]
+[[Category: Grotli M]]
+[[Category: Hyvonen M]]
+[[Category: Lulla A]]
+[[Category: Nain-Perez A]]
+[[Category: Nilsson O]]