Sara C Nilsson
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Explore the profile of Sara C Nilsson including associated specialties, affiliations and a list of published articles.
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22
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Recent Articles
11.
van de Ven J, Nilsson S, Tan P, Buitendijk G, Ristau T, Mohlin F, et al.
Nat Genet
. 2013 May;
45(7):813-7.
PMID: 23685748
Up to half of the heritability of age-related macular degeneration (AMD) is explained by common variants. Here, we report the identification of a rare, highly penetrant missense mutation in CFI...
12.
Foltyn Zadura A, Zipfel P, Bokarewa M, Sturfelt G, Jonsen A, Nilsson S, et al.
Arthritis Res Ther
. 2012 Aug;
14(4):R185.
PMID: 22894814
Introduction: Complement activation is involved in rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and atypical hemolytic uremic syndrome (aHUS). Autoantibodies to complement inhibitor factor H (FH), particularly in association with...
13.
Sanchez-Gallego J, Groeneveld T, Krentz S, Nilsson S, Villoutreix B, Blom A
J Biol Chem
. 2012 Mar;
287(17):13572-83.
PMID: 22393059
Factor I (FI) is a serine protease that inhibits all complement pathways by degrading activated complement components C3b and C4b. FI functions only in the presence of several cofactors, such...
14.
Jonsen A, Nilsson S, Ahlqvist E, Svenungsson E, Gunnarsson I, Eriksson K, et al.
Arthritis Res Ther
. 2011 Dec;
13(6):R206.
PMID: 22171659
Introduction: Inherited deficiencies of several complement components strongly predispose to systemic lupus erythematosus (SLE) while deficiencies of complement inhibitors are found in kidney diseases such as atypical hemolytic uremic syndrome...
15.
Nilsson S, Sim R, Lea S, Fremeaux-Bacchi V, Blom A
Mol Immunol
. 2011 May;
48(14):1611-20.
PMID: 21529951
Factor I (FI) is a crucial inhibitor controlling all complement pathways due to its ability to degrade activated complement proteins C3b and C4b in the presence of cofactors such as...
16.
Nita I, Genel F, Nilsson S, Smart J, Truedsson L, Choo S, et al.
Mol Immunol
. 2011 Feb;
48(8):1068-72.
PMID: 21316765
Factor I (FI) is the major complement inhibitor that degrades activated complement components C3b and C4b in the presence of specific cofactors. Complete FI deficiency results in secondary complement deficiency...
17.
Nilsson S, Nita I, Mansson L, Groeneveld T, Trouw L, Villoutreix B, et al.
J Biol Chem
. 2010 Jan;
285(9):6235-45.
PMID: 20044478
The central complement inhibitor factor I (FI) degrades activated complement factors C4b and C3b in the presence of cofactors such as C4b-binding protein, factor H, complement receptor 1, and membrane...
18.
Bienaime F, Dragon-Durey M, Regnier C, Nilsson S, Kwan W, Blouin J, et al.
Kidney Int
. 2009 Dec;
77(4):339-49.
PMID: 20016463
Genetic studies have shown that mutations of complement inhibitors such as membrane cofactor protein, Factors H, I, or B and C3 predispose patients to atypical hemolytic uremic syndrome (aHUS). Factor...
19.
Nilsson S, Kalchishkova N, Trouw L, Fremeaux-Bacchi V, Villoutreix B, Blom A
Eur J Immunol
. 2009 Oct;
40(1):172-85.
PMID: 19877009
The complement system is regulated by inhibitors such as factor I (FI), a serine protease that degrades activated complement factors C4b and C3b in the presence of specific cofactors. Mutations...
20.
Nilsson S, Trouw L, Renault N, Miteva M, Genel F, Zelazko M, et al.
Eur J Immunol
. 2008 Dec;
39(1):310-23.
PMID: 19065647
Complete deficiency of complement inhibitor factor I (FI) results in secondary complement deficiency due to uncontrolled spontaneous alternative pathway activation leading to susceptibility to infections. Current genetic examination of two...