445 research outputs found
Identification of the Kna/Knb polymorphism and a method for Knops genotyping
No full textDNA mutations resulting in the McCoy and Swain-Langley polymorphisms have been identified on complement receptor 1 (CR1)-a ligand for rosetting of Plasmodium falciparum-infected RBCs. The molecular identification of the Kna/Knb polymorphism was sought to develop a genotyping method for use in the study of the Knops blood group and malaria
CR1 Knops blood group alleles are not associated with severe malaria in the Gambia
No full textThe Knops blood group antigen erythrocyte polymorphisms have been associated with reduced falciparum malaria-based in vitro rosette formation (putative malaria virulence factor). Having previously identified single-nucleotide polymorphisms (SNPs) in the human complement receptor 1 (CR1/CD35) gene underlying the Knops antithetical antigens Sl1/Sl2 and McC(a)/McC(b), we have now performed genotype comparisons to test associations between these two molecular variants and severe malaria in West African children living in the Gambia. While SNPs associated with Sl:2 and McC(b+) were equally distributed among malaria-infected children with severe malaria and control children not infected with malaria parasites, high allele frequencies for Sl 2 (0.800, 1,365/1,706) and McC(b) (0.385, 658/1706) were observed. Further, when compared to the Sl 1/McC(a) allele observed in all populations, the African Sl 2/McC(b) allele appears to have evolved as a result of positive selection (modified Nei-Gojobori test Ka-Ks/s.e.=1.77, P-valu
§ 24
No full textJacoby F. Sicherungsgrundschuld. In: Derleder P, Knops K-O, Bamberger HG, eds. Handbuch zum deutschen und europäischen Bankrecht. 2nd ed. Berlin; 2008: 751-778
§ 18
No full textJacoby F. Sicherungsgrundschuld. In: Derleder P, Knops K-O, Bamberger HG, eds. Handbuch zum deutschen und europäischen Bankrecht. 1st ed. Berlin; 2004: 523-548
Die Inhaltskontrolle des Verwaltervertrags
No full textJacoby F. Die Inhaltskontrolle des Verwaltervertrags. In: Knops K-O, Bamberger HG, Hölzle G, eds. Zivilrecht im Wandel - Festschrift für Peter Derleder zum 75. Geburtstag. Berlin Heidelberg: Springer-Verlag; 2015: 235-246
Bookreview R. Anthone, E. Janssens, S. Vervoort en J. Knops (red.), Peinzen. 49 filosofische vragen voor kinderen, Leuven: Acco, 2006
No full textR. Anthone, E. Janssens, S. Vervoort en J. Knops (red.), Peinzen. 49 filosofische vragen voor kinderen, Leuven: Acco, 200
The impact of decoupled payments on off-farm labour supply : evidence from Ireland and Italy
No full textLack of Evidence from Studies of Soluble Protein Fragments that Knops Blood Group Polymorphisms in Complement Receptor-Type 1 Are Driven by Malaria
No full textComplement receptor-type 1 (CR1, CD35) is the immune-adherence receptor, a complement regulator, and an erythroid receptor for Plasmodium falciparum during merozoite invasion and subsequent rosette formation involving parasitized and non-infected erythrocytes. The non-uniform geographical distribution of Knops blood group CR1 alleles Sl1/2 and McC(a/b) may result from selective pressures exerted by differential exposure to infectious hazards. Here, four variant short recombinant versions of CR1 were produced and analyzed, focusing on complement control protein modules (CCPs) 15-25 of its ectodomain. These eleven modules encompass a region (CCPs 15-17) key to rosetting, opsonin recognition and complement regulation, as well as the Knops blood group polymorphisms in CCPs 24-25. All four CR1 15-25 variants were monomeric and had similar axial ratios. Modules 21 and 22, despite their double-length inter-modular linker, did not lie side-by-side so as to stabilize a bent-back architecture that would facilitate cooperation between key functional modules and Knops blood group antigens. Indeed, the four CR1 15-25 variants had virtually indistinguishable affinities for immobilized complement fragments C3b (K(D) = 0.8-1.1 µM) and C4b (K(D) = 5.0-5.3 µM). They were all equally good co-factors for factor I-catalysed cleavage of C3b and C4b, and they bound equally within a narrow affinity range, to immobilized C1q. No differences between the variants were observed in assays for inhibition of erythrocyte invasion by P. falciparum or for rosette disruption. Neither differences in complement-regulatory functionality, nor interactions with P. falciparum proteins tested here, appear to have driven the non-uniform geographic distribution of these alleles
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