@article{Buchholz.2008,
  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.},
  added-at = {2008-10-14T16:07:18.000+0200},
  author = {Buchholz, Kathrin and Rahlfs, Stefan and Schirmer, Heiner R. and Becker, Katja and Matuschewski, Kai},
  biburl = {http://www.bibsonomy.org/bibtex/288be58900ce4b5c3072293d9fbc91bf8/nutribiochem},
  interhash = {872707ee175822f4914a1a0af2d30325},
  intrahash = {88be58900ce4b5c3072293d9fbc91bf8},
  issn = {1932-6203},
  journal = {PLoS ONE},
  keywords = {Animals Base_Sequence Blotting DNA_Primers IFZ Life_Cycle_Stages Messenger Peroxidases Plasmodium_berghei RNA Rats Reverse_Transcriptase_Polymerase_Chain_Reaction Western},
  number = 6,
  pages = {e2474-e2474},
  timestamp = {2008-10-14T16:07:18.000+0200},
  title = {Depletion of Plasmodium berghei plasmoredoxin reveals a non-essential role for life cycle progression of the malaria parasite},
  volume = 3,
  year = 2008
}