3ula: Difference between revisions

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[[Image:3ula.jpg|left|200px]]
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{{STRUCTURE_3ula|  PDB=3ula  |  SCENE=  }}  
{{STRUCTURE_3ula|  PDB=3ula  |  SCENE=  }}  
===Crystal structure of the TV3 mutant F63W-MD-2-Eritoran complex===
===Crystal structure of the TV3 mutant F63W-MD-2-Eritoran complex===
{{ABSTRACT_PUBMED_22363519}}


==Disease==
[[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> [[http://www.uniprot.org/uniprot/LY96_HUMAN LY96_HUMAN]] Cooperates with TLR4 in the innate immune response to bacterial lipopolysaccharide (LPS), and with TLR2 in the response to cell wall components from Gram-positive and Gram-negative bacteria. Enhances TLR4-dependent activation of NF-kappa-B. Cells expressing both MD2 and TLR4, but not TLR4 alone, respond to LPS.
(as it appears on PubMed at http://www.pubmed.gov), where 22363519 is the PubMed ID number.
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{{ABSTRACT_PUBMED_22363519}}


==About this Structure==
==About this Structure==
[[3ula]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Homo_sapiens,_eptatretus_burgeri Homo sapiens, eptatretus burgeri]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ULA OCA].  
[[3ula]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Eptatretus_burgeri Eptatretus burgeri] and [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ULA OCA].  


==Reference==
==Reference==
<ref group="xtra">PMID:022363519</ref><references group="xtra"/>
<ref group="xtra">PMID:022363519</ref><references group="xtra"/><references/>
[[Category: Eptatretus burgeri]]
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Homo sapiens, eptatretus burgeri]]
[[Category: Cheong, H K.]]
[[Category: Cheong, H K.]]
[[Category: Jeon, Y H.]]
[[Category: Jeon, Y H.]]

Revision as of 19:56, 24 March 2013

Template:STRUCTURE 3ula

Crystal structure of the TV3 mutant F63W-MD-2-Eritoran complexCrystal structure of the TV3 mutant F63W-MD-2-Eritoran complex

Template:ABSTRACT PUBMED 22363519

DiseaseDisease

[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.

FunctionFunction

[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] [LY96_HUMAN] Cooperates with TLR4 in the innate immune response to bacterial lipopolysaccharide (LPS), and with TLR2 in the response to cell wall components from Gram-positive and Gram-negative bacteria. Enhances TLR4-dependent activation of NF-kappa-B. Cells expressing both MD2 and TLR4, but not TLR4 alone, respond to LPS.

About this StructureAbout this Structure

3ula is a 4 chain structure with sequence from Eptatretus burgeri and Homo sapiens. Full crystallographic information is available from OCA.

ReferenceReference

[xtra 1]

  1. Han J, Kim HJ, Lee SC, Hong S, Park K, Jeon YH, Kim D, Cheong HK, Kim HS. Structure-based rational design of a Toll-like receptor 4 (TLR4) decoy receptor with high binding affinity for a target protein. PLoS One. 2012;7(2):e30929. Epub 2012 Feb 17. PMID:22363519 doi:10.1371/journal.pone.0030929
  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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