about
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Association of factor H autoantibodies with deletions of CFHR1, CFHR3, CFHR4, and with mutations in CFH, CFI, CD46, and C3 in patients with atypical hemolytic uremic syndromeTriggering of atypical hemolytic uremic syndrome by influenza A (H1N1).A novel hybrid CFH/CFHR3 gene generated by a microhomology-mediated deletion in familial atypical hemolytic uremic syndrome.Factor I autoantibodies in patients with atypical hemolytic uremic syndrome: disease-associated or an epiphenomenon?Genotype/phenotype correlations in complement factor H deficiency arising from uniparental isodisomy.Standardisation of the factor H autoantibody assay.Autoantibodies to CD59, CD55, CD46 or CD35 are not associated with atypical haemolytic uraemic syndrome (aHUS).A De Novo Deletion in the Regulators of Complement Activation Cluster Producing a Hybrid Complement Factor H/Complement Factor H-Related 3 Gene in Atypical Hemolytic Uremic Syndrome.The role of ADAMTS-13 activity and complement mutational analysis in differentiating acute thrombotic microangiopathiesCharacterization of a factor H mutation that perturbs the alternative pathway of complement in a family with membranoproliferative GN.Determining the population frequency of the CFHR3/CFHR1 deletion at 1q32.Complement: central to innate immunity and bridging to adaptive responses.A CD21 low phenotype, with no evidence of autoantibodies to complement proteins, is consistent with a poor prognosis in CLLSelectivity of C3-opsonin targeted complement inhibitors: A distinct advantage in the protection of erythrocytes from paroxysmal nocturnal hemoglobinuria patients.Molecular cloning, chromosomal localization, expression, and functional characterization of the mouse analogue of human CD59.Increased B cell deletion and significantly reduced auto-antibody titre due to premature expression of human complement receptor 2 (CR2, CD21).Expression of human complement receptor type 2 (CD21) in mice during early B cell development results in a reduction in mature B cells and hypogammaglobulinemia.An extended mini-complement factor H molecule ameliorates experimental C3 glomerulopathy.Defective B cell ontogeny and humoral immune response in mice prematurely expressing human complement receptor 2 (CR2, CD21) is similar to that seen in aging wild type mice.Modulation of the Alternative Pathway of Complement by Murine Factor H-Related Proteins.Factor H autoantibodies in membranoproliferative glomerulonephritis.CD59a deficient mice display reduced B cell activity and antibody production in response to T-dependent antigens.Postpartum aHUS secondary to a genetic abnormality in factor H acquired through liver transplantation.An Engineered Complement Factor H Construct for Treatment of C3 Glomerulopathy.A novel method for direct measurement of complement convertases activity in human serum.CD19 is essential for B cell activation by promoting B cell receptor–antigen microcluster formation in response to membrane-bound ligandRegulation of CD59 expression on K562 cells: effects of phorbol myristate acetate, cross-linking antibody and non-lethal complement attackMechanisms of complement resistance induced by non-lethal complement attack and by growth arrestIntrinsic B cell hypo-responsiveness in mice prematurely expressing human CR2/CD21 during B cell developmentB cells from mice prematurely expressing human complement receptor type 2 are unresponsive to T-dependent antigensLarge-Scale Whole-Genome Sequencing Reveals the Genetic Architecture of Primary Membranoproliferative GN and C3 Glomerulopathy
P50
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P50
description
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Kevin J Marchbank
@ast
Kevin J Marchbank
@en
Kevin J Marchbank
@es
Kevin J Marchbank
@nl
type
label
Kevin J Marchbank
@ast
Kevin J Marchbank
@en
Kevin J Marchbank
@es
Kevin J Marchbank
@nl
prefLabel
Kevin J Marchbank
@ast
Kevin J Marchbank
@en
Kevin J Marchbank
@es
Kevin J Marchbank
@nl
P106
P21
P31
P496
0000-0003-1312-5411