Affected erythrocytes of patients with paroxysmal nocturnal hemoglobinuria are deficient in the complement regulatory protein, decay accelerating factor.
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Paroxysmal nocturnal haemoglobinuria (PNH) is caused by somatic mutations in the PIG-A geneCloning and characterization of cDNAs encoding the complete sequence of decay-accelerating factor of human complementCD59, an LY-6-like protein expressed in human lymphoid cells, regulates the action of the complement membrane attack complex on homologous cellsDelivery of drugs bound to erythrocytes: new avenues for an old intravascular carrierRole of decay-accelerating factor in regulating complement activation on the erythrocyte surface as revealed by gene targetingFunctional properties of membrane cofactor protein of complementInhibition of complement activation on the surface of cells after incorporation of decay-accelerating factor (DAF) into their membranesCharacterization of the complement sensitivity of paroxysmal nocturnal hemoglobinuria erythrocytes.Infectious diseases associated with complement deficiencies.Abnormalities in the expression of CD55 and CD59 surface molecules on peripheral blood cells are not specific to paroxysmal nocturnal hemoglobinuria.Self-nonself discrimination by the complement system.Alkaline phosphatase, defensin gene expression and effect of myeloid cell growth factors in normal and leukemic cells.Leukemia arising out of paroxysmal nocturnal hemoglobinuria.A functional SNP in the regulatory region of the decay-accelerating factor gene associates with extraocular muscle pareses in myasthenia gravis.Heightened complement sensitivity of acquired immunodeficiency syndrome lymphocytes related to diminished expression of decay-accelerating factor.Historical aspects of paroxysmal nocturnal haemoglobinuria: 'defining the disease'.Preferential expression of human Fc gamma RIIIPMN (CD16) in paroxysmal nocturnal hemoglobinuria. Discordant expression of glycosyl phosphatidylinositol-linked proteins.Synthesis of aberrant decay-accelerating factor proteins by affected paroxysmal nocturnal hemoglobinuria leukocytesAltered expression of gangliosides in erythrocytes of paroxysmal nocturnal hemoglobinuriaDr(a-) polymorphism of decay accelerating factor. Biochemical, functional, and molecular characterization and production of allele-specific transfectants.Complement modulation of T cell immune responses during homeostasis and disease.Paroxysmal nocturnal haemoglobinuria with coexisting deficiency of the ninth component of complement: lack of massive haemolytic attack.Presence of the Tn antigen on hematopoietic progenitors from patients with the Tn syndromeInteractions of the platelets in paroxysmal nocturnal hemoglobinuria with complement. Relationship to defects in the regulation of complement and to platelet survival in vivo.Increased expression of complement decay-accelerating factor during activation of human neutrophilsAcute myeloblastic leukemia in paroxysmal nocturnal hemoglobinuria. Evidence of evolution from the abnormal paroxysmal nocturnal hemoglobinuria clone.Isolation and characterization of a membrane protein from normal human erythrocytes that inhibits reactive lysis of the erythrocytes of paroxysmal nocturnal hemoglobinuria.Relationship between the membrane inhibitor of reactive lysis and the erythrocyte phenotypes of paroxysmal nocturnal hemoglobinuriaAbnormality of glycophorin-alpha on paroxysmal nocturnal hemoglobinuria erythrocytes.Decay-accelerating factor regulates T-cell immunity in the context of inflammation by influencing costimulatory molecule expression on antigen-presenting cells.Complement in paroxysmal nocturnal hemoglobinuria: exploiting our current knowledge to improve the treatment landscape.Relationship between decay accelerating factor deficiency, diminished acetylcholinesterase activity, and defective terminal complement pathway restriction in paroxysmal nocturnal hemoglobinuria erythrocytesRetrovirus-induced feline pure red cell aplasia. Hematopoietic progenitors are infected with feline leukemia virus and erythroid burst-forming cells are uniquely sensitive to heterologous complementA new aspect of the molecular pathogenesis of paroxysmal nocturnal hemoglobinuria.Decay-accelerating factor ameliorates systemic autoimmune disease in MRL/lpr mice via both complement-dependent and -independent mechanismsDeletion of decay-accelerating factor (CD55) exacerbates autoimmune disease development in MRL/lpr miceComplement-mediated haemolysis and the role of blood transfusion in paroxysmal nocturnal haemoglobinuria.Retinal Pre-Conditioning by CD59a Knockout Protects against Light-Induced Photoreceptor Degeneration.Specific defect in N-acetylglucosamine incorporation in the biosynthesis of the glycosylphosphatidylinositol anchor in cloned cell lines from patients with paroxysmal nocturnal hemoglobinuria.Distribution of decay-accelerating factor in the peripheral blood of normal individuals and patients with paroxysmal nocturnal hemoglobinuria.
P2860
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P2860
Affected erythrocytes of patients with paroxysmal nocturnal hemoglobinuria are deficient in the complement regulatory protein, decay accelerating factor.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on August 1983
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Affected erythrocytes of patie ...... in, decay accelerating factor.
@en
Affected erythrocytes of patie ...... in, decay accelerating factor.
@nl
type
label
Affected erythrocytes of patie ...... in, decay accelerating factor.
@en
Affected erythrocytes of patie ...... in, decay accelerating factor.
@nl
prefLabel
Affected erythrocytes of patie ...... in, decay accelerating factor.
@en
Affected erythrocytes of patie ...... in, decay accelerating factor.
@nl
P2093
P2860
P356
P1476
Affected erythrocytes of patie ...... in, decay accelerating factor.
@en
P2093
A Nicholson-Weller
K F Austen
S I Rosenfeld
P2860
P304
P356
10.1073/PNAS.80.16.5066
P407
P577
1983-08-01T00:00:00Z