Artemisinin resistance in rodent malaria - mutation in the AP2 adaptor μ-chain suggests involvement of endocytosis and membrane protein trafficking

Gisela Henriques; Axel Martinelli; Louise Rodrigues; Katarzyna Modrzynska; Richard Fawcett; Douglas R Houston; Sofia T Borges; Umberto d'Alessandro; Halidou Tinto; Corine Karema; Paul Hunt; Pedro Cravo

doi:10.1186/1475-2875-12-118

Artemisinin resistance in rodent malaria - mutation in the AP2 adaptor μ-chain suggests involvement of endocytosis and membrane protein trafficking

Gisela Henriques, Axel Martinelli, Louise Rodrigues, Katarzyna Modrzynska, Richard Fawcett, Douglas R Houston, Sofia T Borges, Umberto d'Alessandro, Halidou Tinto, Corine Karema, Paul Hunt, Pedro Cravo

School of Biological Sciences

Research output: Contribution to journal › Article › peer-review

Abstract

The control of malaria, caused by Plasmodium falciparum, is hampered by the relentless evolution of drug resistance. Because artemisinin derivatives are now used in the most effective anti-malarial therapy, resistance to artemisinin would be catastrophic. Indeed, studies suggest that artemisinin resistance has already appeared in natural infections. Understanding the mechanisms of resistance would help to prolong the effective lifetime of these drugs. Genetic markers of resistance are therefore required urgently. Previously, a mutation in a de-ubiquitinating enzyme was shown to confer artemisinin resistance in the rodent malaria parasite Plasmodium chabaudi.

Original language	English
Article number	118
Journal	Malaria Journal
Volume	12
DOIs	https://doi.org/10.1186/1475-2875-12-118
Publication status	Published - 2013

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Henriques, G., Martinelli, A., Rodrigues, L., Modrzynska, K., Fawcett, R., Houston, D. R., Borges, S. T., d'Alessandro, U., Tinto, H., Karema, C., Hunt, P., & Cravo, P. (2013). Artemisinin resistance in rodent malaria - mutation in the AP2 adaptor μ-chain suggests involvement of endocytosis and membrane protein trafficking. Malaria Journal, 12, Article 118. https://doi.org/10.1186/1475-2875-12-118

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title = "Artemisinin resistance in rodent malaria - mutation in the AP2 adaptor μ-chain suggests involvement of endocytosis and membrane protein trafficking",

abstract = "The control of malaria, caused by Plasmodium falciparum, is hampered by the relentless evolution of drug resistance. Because artemisinin derivatives are now used in the most effective anti-malarial therapy, resistance to artemisinin would be catastrophic. Indeed, studies suggest that artemisinin resistance has already appeared in natural infections. Understanding the mechanisms of resistance would help to prolong the effective lifetime of these drugs. Genetic markers of resistance are therefore required urgently. Previously, a mutation in a de-ubiquitinating enzyme was shown to confer artemisinin resistance in the rodent malaria parasite Plasmodium chabaudi.",

author = "Gisela Henriques and Axel Martinelli and Louise Rodrigues and Katarzyna Modrzynska and Richard Fawcett and Houston, \{Douglas R\} and Borges, \{Sofia T\} and Umberto d'Alessandro and Halidou Tinto and Corine Karema and Paul Hunt and Pedro Cravo",

year = "2013",

doi = "10.1186/1475-2875-12-118",

language = "English",

volume = "12",

journal = "Malaria Journal",

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Henriques, G, Martinelli, A, Rodrigues, L, Modrzynska, K, Fawcett, R, Houston, DR, Borges, ST, d'Alessandro, U, Tinto, H, Karema, C, Hunt, P & Cravo, P 2013, 'Artemisinin resistance in rodent malaria - mutation in the AP2 adaptor μ-chain suggests involvement of endocytosis and membrane protein trafficking', Malaria Journal, vol. 12, 118. https://doi.org/10.1186/1475-2875-12-118

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T1 - Artemisinin resistance in rodent malaria - mutation in the AP2 adaptor μ-chain suggests involvement of endocytosis and membrane protein trafficking

AU - Henriques, Gisela

AU - Martinelli, Axel

AU - Rodrigues, Louise

AU - Modrzynska, Katarzyna

AU - Fawcett, Richard

AU - Houston, Douglas R

AU - Borges, Sofia T

AU - d'Alessandro, Umberto

AU - Tinto, Halidou

AU - Karema, Corine

AU - Hunt, Paul

AU - Cravo, Pedro

PY - 2013

Y1 - 2013

N2 - The control of malaria, caused by Plasmodium falciparum, is hampered by the relentless evolution of drug resistance. Because artemisinin derivatives are now used in the most effective anti-malarial therapy, resistance to artemisinin would be catastrophic. Indeed, studies suggest that artemisinin resistance has already appeared in natural infections. Understanding the mechanisms of resistance would help to prolong the effective lifetime of these drugs. Genetic markers of resistance are therefore required urgently. Previously, a mutation in a de-ubiquitinating enzyme was shown to confer artemisinin resistance in the rodent malaria parasite Plasmodium chabaudi.

AB - The control of malaria, caused by Plasmodium falciparum, is hampered by the relentless evolution of drug resistance. Because artemisinin derivatives are now used in the most effective anti-malarial therapy, resistance to artemisinin would be catastrophic. Indeed, studies suggest that artemisinin resistance has already appeared in natural infections. Understanding the mechanisms of resistance would help to prolong the effective lifetime of these drugs. Genetic markers of resistance are therefore required urgently. Previously, a mutation in a de-ubiquitinating enzyme was shown to confer artemisinin resistance in the rodent malaria parasite Plasmodium chabaudi.

U2 - 10.1186/1475-2875-12-118

DO - 10.1186/1475-2875-12-118

M3 - Article

C2 - 23561245

SN - 1475-2875

VL - 12

JO - Malaria Journal

JF - Malaria Journal

M1 - 118

ER -

Artemisinin resistance in rodent malaria - mutation in the AP2 adaptor μ-chain suggests involvement of endocytosis and membrane protein trafficking

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