8ivq: Difference between revisions

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 <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=8ivq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8ivq OCA], [https://pdbe.org/8ivq PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8ivq RCSB], [https://www.ebi.ac.uk/pdbsum/8ivq PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8ivq ProSAT]</span></td></tr>
 </table>
-== Function ==
+<div style="background-color:#fffaf0;">
-[https://www.uniprot.org/uniprot/BIRC6_MOUSE BIRC6_MOUSE] Anti-apoptotic protein which can regulate cell death by controlling caspases and by acting as an E3 ubiquitin-protein ligase. Has an unusual ubiquitin conjugation system in that it could combine in a single polypeptide, ubiquitin conjugating (E2) with ubiquitin ligase (E3) activity, forming a chimeric E2/E3 ubiquitin ligase. Its targets include CASP9 and DIABLO/SMAC. Acts as an inhibitor of CASP3, CASP7 and CASP9. Important regulator for the final stages of cytokinesis. Crucial for normal vesicle targeting to the site of abscission, but also for the integrity of the midbody and the midbody ring, and its striking ubiquitin modification. Required for normal placenta development.<ref>PMID:15300255</ref> <ref>PMID:15485903</ref> <ref>PMID:9628897</ref>
+== Publication Abstract from PubMed ==
+Procaspase 9 is the initiator caspase for apoptosis, but how its levels and activities are maintained remains unclear. The gigantic Inhibitor-of-Apoptosis Protein BIRC6/BRUCE/Apollon inhibits both apoptosis and autophagy by promoting ubiquitylation of proapoptotic factors and the key autophagic protein LC3, respectively. Here we show that BIRC6 forms an anti-parallel U-shaped dimer with multiple previously unannotated domains, including a ubiquitin-like domain, and the proapoptotic factor Smac/DIABLO binds BIRC6 in the central cavity. Notably, Smac outcompetes the effector caspase 3 and the pro-apoptotic protease HtrA2, but not procaspase 9, for binding BIRC6 in cells. BIRC6 also binds LC3 through its LC3-interacting region, probably following dimer disruption of this BIRC6 region. Mutation at LC3 ubiquitylation site promotes autophagy and autophagic degradation of BIRC6. Moreover, induction of autophagy promotes autophagic degradation of BIRC6 and caspase 9, but not of other effector caspases. These results are important to understand how the balance between apoptosis and autophagy is regulated under pathophysiological conditions.
+Molecular mechanisms underlying the BIRC6-mediated regulation of apoptosis and autophagy.,Liu SS, Jiang TX, Bu F, Zhao JL, Wang GF, Yang GH, Kong JY, Qie YF, Wen P, Fan LB, Li NN, Gao N, Qiu XB Nat Commun. 2024 Jan 30;15(1):891. doi: 10.1038/s41467-024-45222-1. PMID:38291026<ref>PMID:38291026</ref>
+From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
+</div>
+<div class="pdbe-citations 8ivq" style="background-color:#fffaf0;"></div>
 == References ==
 <references/>