5tnz
From Proteopedia
(Difference between revisions)
m (Protected "5tnz" [edit=sysop:move=sysop]) |
|||
(3 intermediate revisions not shown.) | |||
Line 1: | Line 1: | ||
- | '''Unreleased structure''' | ||
- | + | ==HtrA2 S142D mutant== | |
+ | <StructureSection load='5tnz' size='340' side='right'caption='[[5tnz]], [[Resolution|resolution]] 1.75Å' scene=''> | ||
+ | == Structural highlights == | ||
+ | <table><tr><td colspan='2'>[[5tnz]] is a 1 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=5TNZ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5TNZ FirstGlance]. <br> | ||
+ | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.75Å</td></tr> | ||
+ | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=MES:2-(N-MORPHOLINO)-ETHANESULFONIC+ACID'>MES</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene></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=5tnz FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5tnz OCA], [https://pdbe.org/5tnz PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5tnz RCSB], [https://www.ebi.ac.uk/pdbsum/5tnz PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5tnz ProSAT]</span></td></tr> | ||
+ | </table> | ||
+ | == Disease == | ||
+ | [https://www.uniprot.org/uniprot/HTRA2_HUMAN HTRA2_HUMAN] Defects in HTRA2 are the cause of Parkinson disease type 13 (PARK13) [MIM:[https://omim.org/entry/610297 610297]. A complex neurodegenerative disorder characterized by bradykinesia, resting tremor, muscular rigidity and postural instability, as well as by a clinically significant response to treatment with levodopa. The pathology involves the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies (intraneuronal accumulations of aggregated proteins), in surviving neurons in various areas of the brain.<ref>PMID:15961413</ref> <ref>PMID:18401856</ref> | ||
+ | == Function == | ||
+ | [https://www.uniprot.org/uniprot/HTRA2_HUMAN HTRA2_HUMAN] Serine protease that shows proteolytic activity against a non-specific substrate beta-casein. Promotes or induces cell death either by direct binding to and inhibition of BIRC proteins (also called inhibitor of apoptosis proteins, IAPs), leading to an increase in caspase activity, or by a BIRC inhibition-independent, caspase-independent and serine protease activity-dependent mechanism. Cleaves THAP5 and promotes its degradation during apoptosis. Isoform 2 seems to be proteolytically inactive.<ref>PMID:15200957</ref> <ref>PMID:19502560</ref> | ||
- | + | ==See Also== | |
- | + | *[[Proteinase 3D structures|Proteinase 3D structures]] | |
- | + | == References == | |
- | [[Category: | + | <references/> |
+ | __TOC__ | ||
+ | </StructureSection> | ||
+ | [[Category: Homo sapiens]] | ||
+ | [[Category: Large Structures]] | ||
+ | [[Category: Macedo-Ribeiro S]] | ||
+ | [[Category: Merski M]] | ||
+ | [[Category: Pereira PJB]] |
Current revision
HtrA2 S142D mutant
|