8e2j: Difference between revisions

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 == Structural highlights ==
 <table><tr><td colspan='2'>[[8e2j]] 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=8E2J OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8E2J FirstGlance]. <br>
-</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=8e2j FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8e2j OCA], [https://pdbe.org/8e2j PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8e2j RCSB], [https://www.ebi.ac.uk/pdbsum/8e2j PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8e2j ProSAT]</span></td></tr>
+</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution|Resolution]] 3.44&#8491;</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=8e2j FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8e2j OCA], [https://pdbe.org/8e2j PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8e2j RCSB], [https://www.ebi.ac.uk/pdbsum/8e2j PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8e2j ProSAT]</span></td></tr>
 </table>
-== Disease ==
+<div style="background-color:#fffaf0;">
-[https://www.uniprot.org/uniprot/DBLOH_HUMAN DBLOH_HUMAN] Defects in DIABLO are the cause of deafness autosomal dominant type 64 (DFNA64) [MIM:[https://omim.org/entry/614152 614152]. DFNA64 is a form of non-syndromic sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information.<ref>PMID:21722859</ref>
+== Publication Abstract from PubMed ==
-== Function ==
+Tight regulation of apoptosis is essential for metazoan development and prevents diseases such as cancer and neurodegeneration. Caspase activation is central to apoptosis, and inhibitor of apoptosis proteins (IAPs) are the principal actors that restrain caspase activity and are therefore attractive therapeutic targets. IAPs, in turn, are regulated by mitochondria-derived proapoptotic factors such as SMAC and HTRA2. Through a series of cryo-electron microscopy structures of full-length human baculoviral IAP repeat-containing protein 6 (BIRC6) bound to SMAC, caspases, and HTRA2, we provide a molecular understanding for BIRC6-mediated caspase inhibition and its release by SMAC. The architecture of BIRC6, together with near-irreversible binding of SMAC, elucidates how the IAP inhibitor SMAC can effectively control a processive ubiquitin ligase to respond to apoptotic stimuli.
-[https://www.uniprot.org/uniprot/DBLOH_HUMAN DBLOH_HUMAN] Promotes apoptosis by activating caspases in the cytochrome c/Apaf-1/caspase-9 pathway. Acts by opposing the inhibitory activity of inhibitor of apoptosis proteins (IAP). Inhibits the activity of BIRC6/bruce by inhibiting its binding to caspases. Isoform 3 attenuates the stability and apoptosis-inhibiting activity of XIAP/BIRC4 by promoting XIAP/BIRC4 ubiquitination and degradation through the ubiquitin-proteasome pathway. Isoform 3 also disrupts XIAP/BIRC4 interacting with processed caspase-9 and promotes caspase-3 activation. Isoform 1 is defective in the capacity to down-regulate the XIAP/BIRC4 abundance.<ref>PMID:10929711</ref> <ref>PMID:14523016</ref> <ref>PMID:15200957</ref>
+Structures of BIRC6-client complexes provide a mechanism of SMAC-mediated release of caspases.,Hunkeler M, Jin CY, Fischer ES Science. 2023 Mar 17;379(6637):1105-1111. doi: 10.1126/science.ade5750. Epub 2023 , Feb 9. PMID:36758104<ref>PMID:36758104</ref>
+From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
+</div>
+<div class="pdbe-citations 8e2j" style="background-color:#fffaf0;"></div>
 == References ==
 <references/>