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Isolation and characterization of factor I of the bovine complement system [PDF]

open access: bronzeAmerican Journal of Veterinary Research, 2003
AbstractObjective—To isolate and characterize factor I of the bovine complement system.Sample Population—Serum obtained from the blood of beef cattle.Procedures—Serum samples were fractionated to yield factor I by means of sequential precipitation, ionexchange, and gel-filtration chromatography.
W. Peter Aston, Marilyn Menger
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In vitro biosynthesis of complement factor I by human endothelial cells

European Journal of Immunology, 1992
AbstractWe have studied the secretion of the complement regulatory protein factor I by human umbilical vein endothelial cells (HUVEC). Northern and Western blot analysis and biosynthetic labeling experiments indicate that HUVEC secrete factor I at very low levels in basal conditions and that this secretion is significantly enhanced by interferon‐γ ...
Hélène Dauchel   +5 more
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The Catalytically Active Serine Protease Domain of Human Complement Factor I

Biochemistry, 2005
Factor I (fI) is a major regulator of complement. As a protease it has very restricted specificity, cleaving only C3b or C4b in the presence of a cofactor such as factor H (fH). Cleavage of C3b by fI yields iC3b, a major opsonin. The cleavage occurs through the formation of a ternary complex between the enzyme, the substrate, and the cofactor.
Xuehui Chen   +6 more
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Glomerulonephritis in a patient with complement factor I deficiency [PDF]

open access: possibleAmerican Journal of Kidney Diseases, 1999
Complement factor I deficiency is known to be associated with recurrent pyogenic infections. The patient described here had recurrent attacks of otitis, sinusitis, and bronchopneumonia since childhood. At the age of 24 years, he had an acute episode of systemic vasculitis with purpura, but no nephritis.
Jean A. Laissue   +4 more
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A Family with Complement Factor I Deficiency

Scandinavian Journal of Immunology, 1986
A family with inherited factor I deficiency is described. The proband was a 19‐year‐old Caucasian female with one episode of meningococcal meningitis and one episode of suspected septicaemia of unknown cause. Two obligate and two probable heterozyotes with factor I levels below the lower limit of the reference range were identified.
J M Rasmussen   +3 more
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Complement Factor I Deficiency With Recurrent Aseptic Meningitis

Archives of Internal Medicine, 1993
Patients with deficiency of the complement regulatory protein factor I typically present with systemic pyogenic bacterial infections, including meningitis. We report a novel case with total deficiency of factor I in serum and plasma; the patient experienced nine consecutive episodes of aseptic meningitis within a 2-year period.
Anita Gewurz   +2 more
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Molecular basis of complement factor I deficiency in Tunisian atypical haemolytic and uraemic syndrome patients

Nephrology, 2019
The aim of the present study was to characterize the molecular basis of complement factor I deficiency in Tunisian atypical haemolytic and uremic syndrome patients with low factor I levels.
Hend Jlajla   +13 more
semanticscholar   +1 more source

[1] Complement factor I and cofactors in control of complement system convertase enzymes

1993
Publisher Summary This chapter describes the complement factor I and cofactors in control of complement system convertase enzymes. Complement factor I was first described and partially characterized in 1966–1968 as an enzyme involved in the physiological degradation of the major complement protein C3.
Sim, R. B.   +3 more
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A new polymorphic variant of human complement factor I

Human Genetics, 1989
Sera from 305 individuals were typed for factor I, and a new variant, tentatively designated FI C, was found. All other samples were FI B except for seven samples from Chinese that were of the FI AB phenotype. This suggests that polymorphism of factor I may be rare in Caucasians.
Bodil Larsen, Ming Zhou
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Complement factor I deficiency in a family with recurrent infections

Immunopharmacology, 1997
Factor I deficiency causes a permanent, uncontrolled activation of the alternative pathway resulting in an increased turnover of C3 and consumption of factor B, factor H and properdin. Factor I deficiency is clinically associated with recurrent bacterial infections already in early infancy, mainly affecting the upper and lower respiratory tract, or ...
Michael Kirschfink   +5 more
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