Properdinproperdin deficiency, properdin
|Gene location Human|
|Chr||X chromosome human|
|Gene location Mouse|
|Chr||X chromosome mouse|
|Band||X A13|X 1644 cM||Start||20,925,454 bp|
|Molecular function|| protein binding|
|Cellular component|| extracellular matrix|
endoplasmic reticulum lumen
specific granule lumen
tertiary granule lumen
|Biological process|| immune response|
regulation of complement activation
defense response to bacterium
immune system process
protein O-linked fucosylation
complement activation, alternative pathway
innate immune response
|Sources:Amigo / QuickGO|
|The alternative pathway is not dependent on antibodies This branch of the complement system is activated by IgA immune complexes and bacterial endotoxins, polysaccharides, and cell walls, and results in producing anaphylatoxins, opsonins, chemotactic factors, and the membrane attack complex, all of which help fight pathogens
Properdin was discovered in 1954 by Dr Louis Pillemer of the Institute of Pathology now the Department of Pathology at Case Western Reserve University
Properdin deficiency is a rare X-linked disease in which properdin is deficient Affected individuals are susceptible to fulminant meningococcal disease
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