Abstract
We previously hypothesized that the key site of chloroquine (CQ) antimalarial action and resistance development is in nucleus of malaria parasite, and that lysosomal (food vacuolar) accumulation of CQ may benefit parasite's survival through reducing the drug pressure on the key site. To further support our hypothesis we propose that Plasmodium falciparum chloroquine resistance marker protein (Pfcrmp) may be a CQ target protein in nucleus and that CQ resistance in malaria parasites may be caused by genetic alterations in Pfcrmp gene.
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