Targeted gene disruption shows that knobs enable malaria-infected red cells to cytoadhere under physiological shear stress

Cell. 1997 Apr 18;89(2):287-96. doi: 10.1016/s0092-8674(00)80207-x.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Blood Platelets / metabolism
  • Blood Proteins / analysis
  • CD36 Antigens / metabolism
  • Cell Adhesion / physiology*
  • Erythrocyte Membrane / chemistry
  • Erythrocyte Membrane / ultrastructure
  • Erythrocytes / cytology*
  • Erythrocytes / parasitology*
  • Gene Expression
  • Molecular Sequence Data
  • Mutagenesis
  • Peptides / genetics
  • Peptides / physiology*
  • Plasmodium falciparum / physiology*
  • Protozoan Proteins / analysis
  • Stress, Mechanical
  • Transfection


  • Blood Proteins
  • CD36 Antigens
  • Peptides
  • Protozoan Proteins
  • erythrocyte membrane protein 1, Plasmodium falciparum
  • knob protein, Plasmodium falciparum

Associated data

  • GENBANK/L40608