2z63

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[[Image:2z63.png|left|200px]]
 
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{{STRUCTURE_2z63| PDB=2z63 | SCENE= }}
{{STRUCTURE_2z63| PDB=2z63 | SCENE= }}
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===Crystal structure of the TV8 hybrid of human TLR4 and hagfish VLRB.61===
===Crystal structure of the TV8 hybrid of human TLR4 and hagfish VLRB.61===
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{{ABSTRACT_PUBMED_17803912}}
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{{ABSTRACT_PUBMED_17803912}}
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==Disease==
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[[http://www.uniprot.org/uniprot/TLR4_HUMAN TLR4_HUMAN]] Genetic variation in TLR4 is associated with age-related macular degeneration type 10 (ARMD10) [MIM:[http://omim.org/entry/611488 611488]]. ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane.
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==Function==
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[[http://www.uniprot.org/uniprot/TLR4_HUMAN TLR4_HUMAN]] Cooperates with LY96 and CD14 to mediate the innate immune response to bacterial lipopolysaccharide (LPS). Acts via MYD88, TIRAP and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Also involved in LPS-independent inflammatory responses triggered by Ni(2+). These responses require non-conserved histidines and are, therefore, species-specific.<ref>PMID:20711192</ref>
==About this Structure==
==About this Structure==
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==Reference==
==Reference==
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<ref group="xtra">PMID:017803912</ref><references group="xtra"/>
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<ref group="xtra">PMID:017803912</ref><references group="xtra"/><references/>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Kim, H M.]]
[[Category: Kim, H M.]]

Revision as of 01:06, 25 March 2013

Template:STRUCTURE 2z63

Contents

Crystal structure of the TV8 hybrid of human TLR4 and hagfish VLRB.61

Template:ABSTRACT PUBMED 17803912

Disease

[TLR4_HUMAN] Genetic variation in TLR4 is associated with age-related macular degeneration type 10 (ARMD10) [MIM:611488]. ARMD is a multifactorial eye disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane.

Function

[TLR4_HUMAN] Cooperates with LY96 and CD14 to mediate the innate immune response to bacterial lipopolysaccharide (LPS). Acts via MYD88, TIRAP and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Also involved in LPS-independent inflammatory responses triggered by Ni(2+). These responses require non-conserved histidines and are, therefore, species-specific.[1]

About this Structure

2z63 is a 1 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA.

See Also

Reference

  • Kim HM, Park BS, Kim JI, Kim SE, Lee J, Oh SC, Enkhbayar P, Matsushima N, Lee H, Yoo OJ, Lee JO. Crystal structure of the TLR4-MD-2 complex with bound endotoxin antagonist Eritoran. Cell. 2007 Sep 7;130(5):906-17. PMID:17803912 doi:http://dx.doi.org/10.1016/j.cell.2007.08.002
  1. ↑ Schmidt M, Raghavan B, Muller V, Vogl T, Fejer G, Tchaptchet S, Keck S, Kalis C, Nielsen PJ, Galanos C, Roth J, Skerra A, Martin SF, Freudenberg MA, Goebeler M. Crucial role for human Toll-like receptor 4 in the development of contact allergy to nickel. Nat Immunol. 2010 Sep;11(9):814-9. doi: 10.1038/ni.1919. Epub 2010 Aug 15. PMID:20711192 doi:10.1038/ni.1919

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OCA

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