3rc5

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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=3rc5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3rc5 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3rc5 RCSB], [http://www.ebi.ac.uk/pdbsum/3rc5 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=3rc5 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3rc5 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3rc5 RCSB], [http://www.ebi.ac.uk/pdbsum/3rc5 PDBsum]</span></td></tr>
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== Function ==
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[[http://www.uniprot.org/uniprot/MAVS_HUMAN MAVS_HUMAN]] Required for innate immune defense against viruses. Acts downstream of DDX58/RIG-I and IFIH1/MDA5, which detect intracellular dsRNA produced during viral replication, to coordinate pathways leading to the activation of NF-kappa-B, IRF3 and IRF7, and to the subsequent induction of antiviral cytokines such as IFN-beta and RANTES (CCL5). Peroxisomal and mitochondrial MAVS act sequentially to create an antiviral cellular state. Upon viral infection, peroxisomal MAVS induces the rapid interferon-independent expression of defense factors that provide short-term protection, whereas mitochondrial MAVS activates an interferon-dependent signaling pathway with delayed kinetics, which amplifies and stabilizes the antiviral response. May activate the same pathways following detection of extracellular dsRNA by TLR3. May protect cells from apoptosis.<ref>PMID:16125763</ref> <ref>PMID:16153868</ref> <ref>PMID:16177806</ref> <ref>PMID:16127453</ref> <ref>PMID:19631370</ref> <ref>PMID:20451243</ref>
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== Publication Abstract from PubMed ==
== Publication Abstract from PubMed ==

Revision as of 17:12, 24 December 2014

Molecular mechanisms of viral and host-cell substrate recognition by HCV NS3/4A protease

3rc5, resolution 1.60Å

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