2vgg: Difference between revisions

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<StructureSection load='2vgg' size='340' side='right'caption='[[2vgg]], [[Resolution|resolution]] 2.74&Aring;' scene=''>
<StructureSection load='2vgg' size='340' side='right'caption='[[2vgg]], [[Resolution|resolution]] 2.74&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[2vgg]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. This structure supersedes the now removed PDB entry [http://oca.weizmann.ac.il/oca-bin/send-pdb?obs=1&id=1liy 1liy]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2VGG OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2VGG FirstGlance]. <br>
<table><tr><td colspan='2'>[[2vgg]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. This structure supersedes the now removed PDB entry [http://oca.weizmann.ac.il/oca-bin/send-pdb?obs=1&id=1liy 1liy]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2VGG OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=2VGG FirstGlance]. <br>
</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=MN:MANGANESE+(II)+ION'>MN</scene>, <scene name='pdbligand=PGA:2-PHOSPHOGLYCOLIC+ACID'>PGA</scene></td></tr>
</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=MN:MANGANESE+(II)+ION'>MN</scene>, <scene name='pdbligand=PGA:2-PHOSPHOGLYCOLIC+ACID'>PGA</scene></td></tr>
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[2vgb|2vgb]], [[2vgf|2vgf]]</div></td></tr>
<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Pyruvate_kinase Pyruvate kinase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.40 2.7.1.40] </span></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=2vgg FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2vgg OCA], [https://pdbe.org/2vgg PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2vgg RCSB], [https://www.ebi.ac.uk/pdbsum/2vgg PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2vgg ProSAT]</span></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=2vgg FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2vgg OCA], [https://pdbe.org/2vgg PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=2vgg RCSB], [https://www.ebi.ac.uk/pdbsum/2vgg PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=2vgg ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
[[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.  
[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.
== Function ==
== Function ==
[[https://www.uniprot.org/uniprot/KPYR_HUMAN KPYR_HUMAN]] Plays a key role in glycolysis (By similarity).  
[https://www.uniprot.org/uniprot/KPYR_HUMAN KPYR_HUMAN] Plays a key role in glycolysis (By similarity).
== Evolutionary Conservation ==
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
[[Image:Consurf_key_small.gif|200px|right]]
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__TOC__
__TOC__
</StructureSection>
</StructureSection>
[[Category: Human]]
[[Category: Homo sapiens]]
[[Category: Large Structures]]
[[Category: Large Structures]]
[[Category: Pyruvate kinase]]
[[Category: Abraham DJ]]
[[Category: Abraham, D J]]
[[Category: Bianchi P]]
[[Category: Bianchi, P]]
[[Category: Chiarelli LR]]
[[Category: Chiarelli, L R]]
[[Category: Dolzan M]]
[[Category: Dolzan, M]]
[[Category: Fortin R]]
[[Category: Fortin, R]]
[[Category: Galizzi A]]
[[Category: Galizzi, A]]
[[Category: Mattevi A]]
[[Category: Mattevi, A]]
[[Category: Valentini G]]
[[Category: Valentini, G]]
[[Category: Wang C]]
[[Category: Wang, C]]
[[Category: Zanella A]]
[[Category: Zanella, A]]
[[Category: Disease mutation]]
[[Category: Glycolysis]]
[[Category: Kinase]]
[[Category: Magnesium]]
[[Category: Metal-binding]]
[[Category: Phosphorylation]]
[[Category: Pyruvate]]
[[Category: Pyruvate kinase in the active r-state]]
[[Category: Transferase]]
Retrieved from "https://proteopedia.org/2vgg"