Control of malarial invasion by phosphorylation of the host cell membrane cytoskeleton.
It has been shown that the entry of the malaria parasite into the red blood cell requires the presence of ATP in the host cell cytoplasm. In red blood cell ghosts that contain no ATP the receptor on the extracellular surface remains in place and parasites will bind to the membrane, but will not enter. ATP is thus necessary for one of the steps in the invasion sequence that follows recognition and attachment. The process of entry appears to involve the active participation of the host cell membrane cytoskeleton. We have suggested that the function of the intracellular ATP may be to regulate phosphorylation of the cytoskeleton. We now present evidence that the activity of the membrane-associated cyclic AMP-independent kinase of the red blood cell is inseparable from invasion; the active substrate may be spectrin.
D000818:Animals; D004910:Erythrocyte Membrane / Q000187:drug effects / Q000469:parasitology*; D006801:Humans; D008565:Membrane Proteins / Q000097:blood*; D010766:Phosphorylation; D010963:Plasmodium falciparum / Q000187:drug effects / Q000472:pathogenicity*; D011494:Protein Kinases / Q000494:pharmacology; D013049:Spectrin / Q000378:metabolism*
D008565:Membrane Proteins; D013049:Spectrin; D011494:Protein Kinases