3hqb

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[[Image:3hqb.png|left|200px]]
 
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{{STRUCTURE_3hqb| PDB=3hqb | SCENE= }}
{{STRUCTURE_3hqb| PDB=3hqb | SCENE= }}
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===Crystal structure of human desarg-C5A===
===Crystal structure of human desarg-C5A===
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{{ABSTRACT_PUBMED_20124699}}
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==Disease==
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[[http://www.uniprot.org/uniprot/CO5_HUMAN CO5_HUMAN]] Defects in C5 are the cause of complement component 5 deficiency (C5D) [MIM:[http://omim.org/entry/609536 609536]]. A rare defect of the complement classical pathway associated with susceptibility to severe recurrent infections, predominantly by Neisseria gonorrhoeae or Neisseria meningitidis. Note=An association study of C5 haplotypes and genotypes in individuals with chronic hepatitis C virus infection shows that individuals homozygous for the C5_1 haplotype have a significantly higher stage of liver fibrosis than individuals carrying at least 1 other allele (PubMed:15995705).
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==Function==
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[[http://www.uniprot.org/uniprot/CO5_HUMAN CO5_HUMAN]] Activation of C5 by a C5 convertase initiates the spontaneous assembly of the late complement components, C5-C9, into the membrane attack complex. C5b has a transient binding site for C6. The C5b-C6 complex is the foundation upon which the lytic complex is assembled. Derived from proteolytic degradation of complement C5, C5 anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes. C5a also stimulates the locomotion of polymorphonuclear leukocytes (chemokinesis) and direct their migration toward sites of inflammation (chemotaxis).
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(as it appears on PubMed at http://www.pubmed.gov), where 20124699 is the PubMed ID number.
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{{ABSTRACT_PUBMED_20124699}}
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==About this Structure==
==About this Structure==
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==Reference==
==Reference==
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<ref group="xtra">PMID:020124699</ref><references group="xtra"/>
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<ref group="xtra">PMID:020124699</ref><references group="xtra"/><references/>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Cook, W J.]]
[[Category: Cook, W J.]]

Revision as of 20:43, 24 March 2013

Template:STRUCTURE 3hqb

Contents

Crystal structure of human desarg-C5A

Template:ABSTRACT PUBMED 20124699

Disease

[CO5_HUMAN] Defects in C5 are the cause of complement component 5 deficiency (C5D) [MIM:609536]. A rare defect of the complement classical pathway associated with susceptibility to severe recurrent infections, predominantly by Neisseria gonorrhoeae or Neisseria meningitidis. Note=An association study of C5 haplotypes and genotypes in individuals with chronic hepatitis C virus infection shows that individuals homozygous for the C5_1 haplotype have a significantly higher stage of liver fibrosis than individuals carrying at least 1 other allele (PubMed:15995705).

Function

[CO5_HUMAN] Activation of C5 by a C5 convertase initiates the spontaneous assembly of the late complement components, C5-C9, into the membrane attack complex. C5b has a transient binding site for C6. The C5b-C6 complex is the foundation upon which the lytic complex is assembled. Derived from proteolytic degradation of complement C5, C5 anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes. C5a also stimulates the locomotion of polymorphonuclear leukocytes (chemokinesis) and direct their migration toward sites of inflammation (chemotaxis).

About this Structure

3hqb is a 2 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA.

Reference

  • Cook WJ, Galakatos N, Boyar WC, Walter RL, Ealick SE. Structure of human desArg-C5a. Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):190-7. Epub 2010 Jan 22. PMID:20124699 doi:10.1107/S0907444909049051

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OCA

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