6nvb: Difference between revisions
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<StructureSection load='6nvb' size='340' side='right'caption='[[6nvb]], [[Resolution|resolution]] 1.64Å' scene=''> | <StructureSection load='6nvb' size='340' side='right'caption='[[6nvb]], [[Resolution|resolution]] 1.64Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[6nvb]] is a 4 chain structure with sequence from [ | <table><tr><td colspan='2'>[[6nvb]] is a 4 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=6NVB OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6NVB FirstGlance]. <br> | ||
</td></tr><tr id=' | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.636Å</td></tr> | ||
<tr id=' | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></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=6nvb FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6nvb OCA], [https://pdbe.org/6nvb PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6nvb RCSB], [https://www.ebi.ac.uk/pdbsum/6nvb PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6nvb ProSAT]</span></td></tr> | ||
</table> | </table> | ||
== Disease == | == Disease == | ||
[ | [https://www.uniprot.org/uniprot/KLK4_HUMAN KLK4_HUMAN] Defects in KLK4 are the cause of amelogenesis imperfecta hypomaturation type 2A1 (AI2A1) [MIM:[https://omim.org/entry/204700 204700]. AI2A1 is an autosomal recessive defect of enamel formation. The disorder involves both primary and secondary dentitions. The teeth have a shiny agar jelly appearance and the enamel is softer than normal. Brown pigment is present in middle layers of enamel.<ref>PMID:15235027</ref> | ||
== Function == | == Function == | ||
[ | [https://www.uniprot.org/uniprot/KLK4_HUMAN KLK4_HUMAN] Involved in enamel formation.<ref>PMID:15235027</ref> | ||
<div style="background-color:#fffaf0;"> | <div style="background-color:#fffaf0;"> | ||
== Publication Abstract from PubMed == | == Publication Abstract from PubMed == | ||
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</div> | </div> | ||
<div class="pdbe-citations 6nvb" style="background-color:#fffaf0;"></div> | <div class="pdbe-citations 6nvb" style="background-color:#fffaf0;"></div> | ||
==See Also== | |||
*[[Kallikrein 3D structures|Kallikrein 3D structures]] | |||
== References == | == References == | ||
<references/> | <references/> | ||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: | [[Category: Homo sapiens]] | ||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: Buckle | [[Category: Buckle AM]] | ||
[[Category: McGowan | [[Category: McGowan S]] | ||
[[Category: Riley | [[Category: Riley BT]] | ||
Latest revision as of 10:00, 11 October 2023
Crystal structure of the inhibitor-free form of the serine protease kallikrein-4Crystal structure of the inhibitor-free form of the serine protease kallikrein-4
Structural highlights
DiseaseKLK4_HUMAN Defects in KLK4 are the cause of amelogenesis imperfecta hypomaturation type 2A1 (AI2A1) [MIM:204700. AI2A1 is an autosomal recessive defect of enamel formation. The disorder involves both primary and secondary dentitions. The teeth have a shiny agar jelly appearance and the enamel is softer than normal. Brown pigment is present in middle layers of enamel.[1] FunctionKLK4_HUMAN Involved in enamel formation.[2] Publication Abstract from PubMedKallikrein 4 (KLK4) is a serine protease that is predominantly expressed in the prostate and is overexpressed in prostate cancer. As such, it has gained attention as an attractive target for prostate cancer therapeutics. Currently, only liganded structures of KLK4 exist in the Protein Data Bank. Until now, inferences about the subtle structural changes in KLK4 upon ligand binding have been made by comparison to other liganded forms, rather than to an apo form. In this study, an inhibitor-free form of KLK4 was crystallized. The crystals obtained belonged to space group P1, contained four molecules in the asymmetric unit and diffracted to 1.64 A resolution. Interestingly, a nonstandard rotamer of the specificity-determining residue Asp189 was observed in all chains. This model will provide a useful unliganded structure for the future structure-guided design of KLK4 inhibitors. Crystal structure of the inhibitor-free form of the serine protease kallikrein-4.,Riley BT, Hoke DE, McGowan S, Buckle AM Acta Crystallogr F Struct Biol Commun. 2019 Aug 1;75(Pt 8):543-546. doi:, 10.1107/S2053230X19009610. Epub 2019 Jul 16. PMID:31397325[3] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. See AlsoReferences
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