期刊
MOLECULAR CELL
卷 6, 期 4, 页码 861-871出版社
CELL PRESS
DOI: 10.1016/S1097-2765(05)00077-8
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资金
- NIAID NIH HHS [R01 AI050234, R37 AI050234, R01 AI050234-01] Funding Source: Medline
The determinant of verapamil-reversible chloroquine resistance (CQR) in a Plasmodium falciparum genetic cross maps to a 36 kb segment of chromosome 7. This segment harbors a 13-exon gene, pfcrt, having point mutations that associate completely with CQR in parasite lines from Asia, Africa, and South America. These data, transfection results, and selection of a CQR line harboring a novel K761 mutation point to a central role for the PfCRT protein in CQR. This transmembrane protein localizes to the parasite digestive vacuole (DV), the site of Co action, where increased compartment acidification associates with PfCRT point mutations. Mutations in PfCRT may result in altered chloroquine flux or reduced drug binding to hematin through an effect on DV pH.
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