1h2p
From Proteopedia
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|ACTIVITY= | |ACTIVITY= | ||
|GENE= | |GENE= | ||
| + | |DOMAIN= | ||
| + | |RELATEDENTRY= | ||
| + | |RESOURCES=<span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1h2p FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1h2p OCA], [http://www.ebi.ac.uk/pdbsum/1h2p PDBsum], [http://www.rcsb.org/pdb/explore.do?structureId=1h2p RCSB]</span> | ||
}} | }} | ||
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==Overview== | ==Overview== | ||
Decay-accelerating factor (CD55), a regulator of the alternative and classical pathways of complement activation, is expressed on all serum-exposed cells. It is used by pathogens, including many enteroviruses and uropathogenic Escherichia coli, as a receptor prior to infection. We describe the x-ray structure of a pathogen-binding fragment of human CD55 at 1.7 A resolution containing two of the three domains required for regulation of human complement. We have used mutagenesis to map biological functions onto the molecule; decay-accelerating activity maps to a single face of the molecule, whereas bacterial and viral pathogens recognize a variety of different sites on CD55. | Decay-accelerating factor (CD55), a regulator of the alternative and classical pathways of complement activation, is expressed on all serum-exposed cells. It is used by pathogens, including many enteroviruses and uropathogenic Escherichia coli, as a receptor prior to infection. We describe the x-ray structure of a pathogen-binding fragment of human CD55 at 1.7 A resolution containing two of the three domains required for regulation of human complement. We have used mutagenesis to map biological functions onto the molecule; decay-accelerating activity maps to a single face of the molecule, whereas bacterial and viral pathogens recognize a variety of different sites on CD55. | ||
| - | |||
| - | ==Disease== | ||
| - | Known diseases associated with this structure: Blood group Cromer OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=125240 125240]], Blood group, Knops system OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=120620 120620]], CR1 deficiency OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=120620 120620]], Malaria, severe, resistance to OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=120620 120620]], SLE susceptibility OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=120620 120620]] | ||
==About this Structure== | ==About this Structure== | ||
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[[Category: ligand for cd97]] | [[Category: ligand for cd97]] | ||
| - | ''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on | + | ''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Sun Mar 30 20:56:32 2008'' |
Revision as of 17:56, 30 March 2008
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| , resolution 2.8Å | |||||||
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| Resources: | FirstGlance, OCA, PDBsum, RCSB | ||||||
| Coordinates: | save as pdb, mmCIF, xml | ||||||
HUMAN CD55 DOMAINS 3 & 4
Overview
Decay-accelerating factor (CD55), a regulator of the alternative and classical pathways of complement activation, is expressed on all serum-exposed cells. It is used by pathogens, including many enteroviruses and uropathogenic Escherichia coli, as a receptor prior to infection. We describe the x-ray structure of a pathogen-binding fragment of human CD55 at 1.7 A resolution containing two of the three domains required for regulation of human complement. We have used mutagenesis to map biological functions onto the molecule; decay-accelerating activity maps to a single face of the molecule, whereas bacterial and viral pathogens recognize a variety of different sites on CD55.
About this Structure
1H2P is a Single protein structure of sequence from Homo sapiens. Full crystallographic information is available from OCA.
Reference
Mapping CD55 function. The structure of two pathogen-binding domains at 1.7 A., Williams P, Chaudhry Y, Goodfellow IG, Billington J, Powell R, Spiller OB, Evans DJ, Lea S, J Biol Chem. 2003 Mar 21;278(12):10691-6. Epub 2002 Dec 22. PMID:12499389
Page seeded by OCA on Sun Mar 30 20:56:32 2008
Categories: Homo sapiens | Single protein | Billington, J. | Chaudhry, Y. | Evans, D J. | Goodfellow, I. | Lea, S M. | Spiller, B. | Williams, P. | Alternative splicing | Bacterial receptor | Complement decay accelerating factor | Complement pathway | Enteroviral receptor | Gpi-anchor | Ligand for cd97
