Journalartikel

Jahr der Veröffentlichung: 2008

Seiten: e2474-

Zeitschrift: PLoS ONE

Bandnummer: 3

Heftnummer: 6

ISSN: 1932-6203

eISSN: 1932-6203

Open Access Status: Gold

DOI Link: https://doi.org/10.1371/journal.pone.0002474

Verlag: Public Library of Science

Abstract: 
Proliferation of the pathogenic Plasmodium asexual blood stages in host erythrocytes requires an exquisite capacity to protect the malaria parasite against oxidative stress. This function is achieved by a complex antioxidant defence system composed of redox-active proteins and low MW antioxidants. Here, we disrupted the P. berghei plasmoredoxin gene that encodes a parasite-specific 22 kDa member of the thioredoxin superfamily. The successful generation of plasmoredoxin knockout mutants in the rodent model malaria parasite and phenotypic analysis during life cycle progression revealed a non-vital role in vivo. Our findings suggest that plasmoredoxin fulfils a specialized and dispensable role for Plasmodium and highlights the need for target validation to inform drug development strategies.

Harvard-Zitierstil: Buchholz, K., Rahlfs, S., Schirmer, R., Becker, K. and Matuschewski, K. (2008) Depletion of Plasmodium berghei Plasmoredoxin Reveals a Non-Essential Role for Life Cycle Progression of the Malaria Parasite, PLoS ONE, 3(6), p. e2474. https://doi.org/10.1371/journal.pone.0002474

APA-Zitierstil: Buchholz, K., Rahlfs, S., Schirmer, R., Becker, K., & Matuschewski, K. (2008). Depletion of Plasmodium berghei Plasmoredoxin Reveals a Non-Essential Role for Life Cycle Progression of the Malaria Parasite. PLoS ONE. 3(6), e2474. https://doi.org/10.1371/journal.pone.0002474