1w0r: Difference between revisions
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{{STRUCTURE_1w0r| PDB=1w0r | SCENE= }} | {{STRUCTURE_1w0r| PDB=1w0r | SCENE= }} | ||
===SOLUTION STRUCTURE OF DIMERIC FORM OF PROPERDIN BY X-RAY SOLUTION SCATTERING AND ANALYTICAL ULTRACENTRIFUGATION=== | |||
{{ABSTRACT_PUBMED_15491616}} | |||
== | ==Disease== | ||
[[http://www.uniprot.org/uniprot/PROP_HUMAN PROP_HUMAN]] Defects in CFP are the cause of properdin deficiency (PFD) [MIM:[http://omim.org/entry/312060 312060]]. PFD results in higher susceptibility to bacterial infections; especially to meningococcal infections. Three phenotypes have been reported: complete deficiency (type I), incomplete deficiency (type II), and dysfunction of properdin (type III).<ref>PMID:8871668</ref><ref>PMID:9710744</ref><ref>PMID:10909851</ref> | |||
==Function== | |||
[[http://www.uniprot.org/uniprot/PROP_HUMAN PROP_HUMAN]] A positive regulator of the alternate pathway of complement. It binds to and stabilizes the C3- and C5-convertase enzyme complexes. | |||
==About this Structure== | ==About this Structure== | ||
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==Reference== | ==Reference== | ||
<ref group="xtra">PMID:015491616</ref><references group="xtra"/> | <ref group="xtra">PMID:015491616</ref><references group="xtra"/><references/> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Perkins, S J.]] | [[Category: Perkins, S J.]] | ||
