Unknown,Transcriptomics,Genomics,Proteomics

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Epigenetic marks reduce erythrocyte uptake of antimalarials

ABSTRACT: Acquired antimalarial drug resistance produces treatment failures and has led to periods of global disease resurgence. In P. falciparum, resistance is known to arise through genome-level changes such as mutations and gene duplications. We now report an epigenetic resistance mechanism involving genes responsible for the plasmodial surface anion channel, a nutrient channel that also transports ions and antimalarial compounds at the host erythrocyte membrane. Two blasticidin S-resistant lines exhibited markedly reduced expression of clag Mutant FCB-br1 and wild-type FCB samples were hybridized to seven arrays (biological repeats) using forward (n=2) and reverse (n=5) fluoro.

ORGANISM(S): Plasmodium falciparum

SUBMITTER: Sanjay Desai

PROVIDER: E-GEOD-47579 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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An epigenetic antimalarial resistance mechanism involving parasite genes linked to nutrient uptake.

Sharma Paresh P Wollenberg Kurt K Sellers Morgan M Zainabadi Kayvan K Galinsky Kevin K Moss Eli E Nguitragool Wang W Neafsey Daniel D Desai Sanjay A SA

The Journal of biological chemistry 20130528 27

Acquired antimalarial drug resistance produces treatment failures and has led to periods of global disease resurgence. In Plasmodium falciparum, resistance is known to arise through genome-level changes such as mutations and gene duplications. We now report an epigenetic resistance mechanism involving genes responsible for the plasmodial surface anion channel, a nutrient channel that also transports ions and antimalarial compounds at the host erythrocyte membrane. Two blasticidin S-resistant lin ...[more]

PMID: 23720749

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Epigenetic marks reduce erythrocyte uptake of antimalarials

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An epigenetic antimalarial resistance mechanism involving parasite genes linked to nutrient uptake.

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