Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.
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Recent advances in the understanding and management of IgA nephropathyCurrent Understanding of the Role of Complement in IgA NephropathyA new paradigm: Diagnosis and management of HSCT-associated thrombotic microangiopathy as multi-system endothelial injuryComplement factor H gene associations with end-stage kidney disease in African Americans.Factors determining penetrance in familial atypical haemolytic uraemic syndrome.The major autoantibody epitope on factor H in atypical hemolytic uremic syndrome is structurally different from its homologous site in factor H-related protein 1, supporting a novel model for induction of autoimmunity in this disease.An international consensus approach to the management of atypical hemolytic uremic syndrome in children.Anti-complement-factor H-associated glomerulopathies.The genetics and immunobiology of IgA nephropathy.Competition between antagonistic complement factors for a single protein on N. meningitidis rules disease susceptibilityComplement Factor H-Related Protein 3 Serum Levels Are Low Compared to Factor H and Mainly Determined by Gene Copy Number Variation in CFHR3Periodontal disease bacteria specific to tonsil in IgA nephropathy patients predicts the remission by the treatment.Association among Complement Factor H Autoantibodies, Deletions of CFHR, and the Risk of Atypical Hemolytic Uremic Syndrome.The complement factor H-related proteins.Plasma levels of complement activation fragments C3b and sC5b-9 significantly increased in patients with thrombotic microangiopathy after allogeneic stem cell transplantation.The Plasmodium falciparum blood stages acquire factor H family proteins to evade destruction by human complement.Factor H autoantibody is associated with atypical hemolytic uremic syndrome in children in the United Kingdom and IrelandDeletion Variants of CFHR1 and CFHR3 Associate with Mesangial Immune Deposits but Not with Progression of IgA Nephropathy.Complement Factor H-Related Protein 4A Is the Dominant Circulating Splice Variant of CFHR4.
P2860
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P2860
Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.
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2013 թուականի Ապրիլին հրատարակուած գիտական յօդուած
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2013 թվականի ապրիլին հրատարակված գիտական հոդված
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2013年の論文
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2013年論文
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2013年論文
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2013年論文
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2013年論文
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2013年論文
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2013年论文
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name
Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.
@ast
Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.
@en
Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.
@nl
type
label
Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.
@ast
Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.
@en
Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.
@nl
prefLabel
Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.
@ast
Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.
@en
Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.
@nl
P2093
P2860
P1433
P1476
Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.
@en
P2093
Heather J Cordell
Iain Moore
Judith A Goodship
Lisa Strain
Lucy V Holmes
Scott J Staniforth
Timothy H J Goodship
P2860
P304
P356
10.1371/JOURNAL.PONE.0060352
P407
P577
2013-04-16T00:00:00Z