3rc4: Difference between revisions
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{{STRUCTURE_3rc4| PDB=3rc4 | SCENE= }} | {{STRUCTURE_3rc4| PDB=3rc4 | SCENE= }} | ||
===Molecular mechanisms of viral and host-cell substrate recognition by HCV NS3/4A protease=== | ===Molecular mechanisms of viral and host-cell substrate recognition by HCV NS3/4A protease=== | ||
{{ABSTRACT_PUBMED_21507982}} | |||
==Disease== | |||
[[http://www.uniprot.org/uniprot/TCAM1_HUMAN TCAM1_HUMAN]] Herpetic encephalitis. Herpes simplex encephalitis 4 (HSE4) [MIM:[http://omim.org/entry/614850 614850]]: A rare complication of human herpesvirus 1 (HHV-1) infection, occurring in only a small minority of HHV-1 infected individuals. HSE is characterized by hemorrhagic necrosis of parts of the temporal and frontal lobes. Onset is over several days and involves fever, headache, seizures, stupor, and often coma, frequently with a fatal outcome. Note=Disease susceptibility is associated with variations affecting the gene represented in this entry.<ref>PMID:22105173</ref> | |||
==Function== | |||
[[http://www.uniprot.org/uniprot/TCAM1_HUMAN TCAM1_HUMAN]] Involved in innate immunity against invading pathogens. Adapter used by TLR3 and TLR4 (through TICAM2) to mediate NF-kappa-B and interferon-regulatory factor (IRF) activation, and to induce apoptosis. Ligand binding to these receptors results in TRIF recruitment through its TIR domain. Distinct protein-interaction motifs allow recruitment of the effector proteins TBK1, TRAF6 and RIPK1, which in turn, lead to the activation of transcription factors IRF3 and IRF7, NF-kappa-B and FADD respectively.<ref>PMID:12471095</ref> <ref>PMID:12539043</ref> <ref>PMID:14739303</ref> | |||
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==About this Structure== | ==About this Structure== | ||
| Line 22: | Line 13: | ||
==Reference== | ==Reference== | ||
<ref group="xtra">PMID:021507982</ref><references group="xtra"/> | <ref group="xtra">PMID:021507982</ref><references group="xtra"/><references/> | ||
[[Category: Hepatitis c virus subtype 1a]] | [[Category: Hepatitis c virus subtype 1a]] | ||
[[Category: Romano, K P.]] | [[Category: Romano, K P.]] | ||
[[Category: Schiffer, C A.]] | [[Category: Schiffer, C A.]] | ||
[[Category: Chymotrypsin-like]] | |||
[[Category: Drug design]] | |||
[[Category: Drug resistance]] | |||
[[Category: Hydrolase]] | |||
[[Category: Hydrolase-hydrolase inhibitor complex]] | |||
[[Category: Protease inhibitor]] | |||
[[Category: Serine protease]] | |||
Revision as of 10:51, 16 May 2013
Molecular mechanisms of viral and host-cell substrate recognition by HCV NS3/4A proteaseMolecular mechanisms of viral and host-cell substrate recognition by HCV NS3/4A protease
Template:ABSTRACT PUBMED 21507982
DiseaseDisease
[TCAM1_HUMAN] Herpetic encephalitis. Herpes simplex encephalitis 4 (HSE4) [MIM:614850]: A rare complication of human herpesvirus 1 (HHV-1) infection, occurring in only a small minority of HHV-1 infected individuals. HSE is characterized by hemorrhagic necrosis of parts of the temporal and frontal lobes. Onset is over several days and involves fever, headache, seizures, stupor, and often coma, frequently with a fatal outcome. Note=Disease susceptibility is associated with variations affecting the gene represented in this entry.[1]
FunctionFunction
[TCAM1_HUMAN] Involved in innate immunity against invading pathogens. Adapter used by TLR3 and TLR4 (through TICAM2) to mediate NF-kappa-B and interferon-regulatory factor (IRF) activation, and to induce apoptosis. Ligand binding to these receptors results in TRIF recruitment through its TIR domain. Distinct protein-interaction motifs allow recruitment of the effector proteins TBK1, TRAF6 and RIPK1, which in turn, lead to the activation of transcription factors IRF3 and IRF7, NF-kappa-B and FADD respectively.[2] [3] [4]
About this StructureAbout this Structure
3rc4 is a 2 chain structure with sequence from Hepatitis c virus subtype 1a. Full crystallographic information is available from OCA.
ReferenceReference
- ↑ Romano KP, Laine JM, Deveau LM, Cao H, Massi F, Schiffer CA. Molecular mechanisms of viral and host-cell substrate recognition by HCV NS3/4A protease. J Virol. 2011 Apr 20. PMID:21507982 doi:10.1128/JVI.00377-11
- ↑ Sancho-Shimizu V, Perez de Diego R, Lorenzo L, Halwani R, Alangari A, Israelsson E, Fabrega S, Cardon A, Maluenda J, Tatematsu M, Mahvelati F, Herman M, Ciancanelli M, Guo Y, AlSum Z, Alkhamis N, Al-Makadma AS, Ghadiri A, Boucherit S, Plancoulaine S, Picard C, Rozenberg F, Tardieu M, Lebon P, Jouanguy E, Rezaei N, Seya T, Matsumoto M, Chaussabel D, Puel A, Zhang SY, Abel L, Al-Muhsen S, Casanova JL. Herpes simplex encephalitis in children with autosomal recessive and dominant TRIF deficiency. J Clin Invest. 2011 Dec;121(12):4889-902. doi: 10.1172/JCI59259. Epub 2011 Nov, 21. PMID:22105173 doi:10.1172/JCI59259
- ↑ Yamamoto M, Sato S, Mori K, Hoshino K, Takeuchi O, Takeda K, Akira S. Cutting edge: a novel Toll/IL-1 receptor domain-containing adapter that preferentially activates the IFN-beta promoter in the Toll-like receptor signaling. J Immunol. 2002 Dec 15;169(12):6668-72. PMID:12471095
- ↑ Oshiumi H, Matsumoto M, Funami K, Akazawa T, Seya T. TICAM-1, an adaptor molecule that participates in Toll-like receptor 3-mediated interferon-beta induction. Nat Immunol. 2003 Feb;4(2):161-7. Epub 2003 Jan 21. PMID:12539043 doi:10.1038/ni886
- ↑ Han KJ, Su X, Xu LG, Bin LH, Zhang J, Shu HB. Mechanisms of the TRIF-induced interferon-stimulated response element and NF-kappaB activation and apoptosis pathways. J Biol Chem. 2004 Apr 9;279(15):15652-61. Epub 2004 Jan 22. PMID:14739303 doi:10.1074/jbc.M311629200