Plasmodium Falciparum is a parasite causing malaria. This pathogen invades red blood cells and exports into them hundreds of its own proteins. In this way, the parasite assembles in the host cells the molecular structures that are necessary to harvest nutrients and escape the immune response. Two new studies revealed that the export of Plasmodium Falciparum’s proteins into red blood cells occurs trough a multi-protein complex known as PTEX (Plasmodium translocon of exported protein).
Tania de Koning-Ward, Deakin University, Waurn Ponds, Australia, and colleagues demonstrated that Plasmodium Falciparum strains lacking a functional PTEX fail to transport their proteins into the host cells and ultimately to replicate. Similar results were obtained in an independent study conducted by Daniel Goldberg, Washington University School of Medicine, St. Louis, USA, and colleagues. PTEX, thus, guarantees Plasmodium falciparum’s survival and, as a consequence, the development of drugs inhibiting its activity may help treat malaria.
- PTEX component HSP101 mediates export of diverse malaria effectors into host erythrocytes
Josh R. Beck, Vasant Muralidharan, Anna Oksman, Daniel E. Goldberg
- PTEX is an essential nexus for protein export in malaria parasites,
Brendan Elsworth, Kathryn Matthews, Catherine Q. Nie, Ming Kalanon, Sarah C. Charnaud, Paul R. Sanders, Scott A. Chisholm, Natalie A. Counihan, Philip J. Shaw, Paco Pino, Jo-Anne Chan, Mauro F. Azevedo, Stephen J. Rogerson, James G. Beeson, Brendan S. Crabb, Paul R. Gilson, Tania F. de Koning-Ward,