4br1: Difference between revisions
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<StructureSection load='4br1' size='340' side='right'caption='[[4br1]], [[Resolution|resolution]] 1.90Å' scene=''> | <StructureSection load='4br1' size='340' side='right'caption='[[4br1]], [[Resolution|resolution]] 1.90Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[4br1]] is a 2 chain structure with sequence from [ | <table><tr><td colspan='2'>[[4br1]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4BR1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4BR1 FirstGlance]. <br> | ||
</td></tr><tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[ | </td></tr><tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Triose-phosphate_isomerase Triose-phosphate isomerase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=5.3.1.1 5.3.1.1] </span></td></tr> | ||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=4br1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4br1 OCA], [https://pdbe.org/4br1 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4br1 RCSB], [https://www.ebi.ac.uk/pdbsum/4br1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4br1 ProSAT]</span></td></tr> | ||
</table> | </table> | ||
== Disease == | == Disease == | ||
[[ | [[https://www.uniprot.org/uniprot/TPIS_HUMAN TPIS_HUMAN]] Defects in TPI1 are the cause of triosephosphate isomerase deficiency (TPI deficiency) [MIM:[https://omim.org/entry/190450 190450]]. TPI deficiency is an autosomal recessive disorder. It is the most severe clinical disorder of glycolysis. It is associated with neonatal jaundice, chronic hemolytic anemia, progressive neuromuscular dysfunction, cardiomyopathy and increased susceptibility to infection. | ||
==See Also== | ==See Also== | ||
*[[Triose | *[[Triose phosphate isomerase 3D structures|Triose phosphate isomerase 3D structures]] | ||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> |