Targeted gene disruption shows that knobs enable malaria-infected red cells to cytoadhere under physiological shear stress
- Author(s)
- Crabb, BS; Cooke, BM; Reeder, JC; Waller, RF; Caruana, SR; Davern, KM; Wickham, ME; Brown, GV; Coppel, RL; Cowman, AF;
- Details
- Publication Year 1997-04-18,Volume 89,Issue #2,Page 287-296
- Journal Title
- CELL
- Publication Type
- Journal Article
- Abstract
- Knobs at the surface of erythrocytes infected with Plasmodium falciparum have been proposed to be important in adherence of these cells to the vascular endothelium. This structure contains the knob-associated histidine-rich protein (KAHRP) and the adhesion receptor P. falciparum erythrocyte membrane protein 1. We have disrupted the gene encoding KAHRP and show that it is essential for knob formation. Knob transfectants adhere to CD36 in static assays; when tested under flow conditions that mimic those of postcapillary venules, however, the binding to CD36 was dramatically reduced. These data suggest that knobs on P. falciparum-infected erythrocytes exert an important influence on adherence of parasitized-erythrocytes to microvascular endothelium, an important process in the pathogenesis of P. falciparum infections.
- Publisher
- CELL PRESS
- Keywords
- HISTIDINE-RICH PROTEIN; HUMAN CEREBRAL MALARIA; PLASMODIUM-FALCIPARUM; ADHESION MOLECULE-1; KNOBLESS CLONE; ANTIGEN CD36; BLOOD-CELLS; CDNA CLONE; ERYTHROCYTES; MEMBRANE
- Publisher's Version
- https://doi.org/10.1016/S0092-8674(00)80207-X
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1997-04-18 12:00:00