3siq

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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3siq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3siq OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3siq RCSB], [http://www.ebi.ac.uk/pdbsum/3siq PDBsum]</span></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3siq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3siq OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3siq RCSB], [http://www.ebi.ac.uk/pdbsum/3siq PDBsum]</span></td></tr>
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== Function ==
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[[http://www.uniprot.org/uniprot/IAP1_DROME IAP1_DROME]] Anti-apoptotic protein which functions as a caspase regulator, using its E3 ubiquitin-protein ligase activity to smother caspase activity. Binds, ubiquitinates and inactivates initiator caspase Nc, and effector caspases ICE and DCP-1. Acts as a NEDD8-E3 ubiquitin-protein ligase for ICE. Suppresses apoptosis by targeting the apoptosome for ubiquitination and inactivation. Plays an important role in cell motility. Overexpression suppresses rpr and W-dependent cell death in the eye. Interaction of th with Nc is required to suppress Nc-mediated cell death; th-mediated ubiquitination of Nc. Acts as a positive regulator of Wnt signaling.<ref>PMID:8548811</ref> <ref>PMID:17397804</ref> <ref>PMID:18259196</ref> <ref>PMID:21145488</ref> <ref>PMID:22304967</ref> <ref>PMID:14517550</ref>
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== Publication Abstract from PubMed ==
== Publication Abstract from PubMed ==

Revision as of 21:35, 24 December 2014

Crystal Structure of autoinhibited dIAP1-BIR1 domain

3siq, resolution 2.40Å

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