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Blood, 1 February 2007, Vol. 109, No. 3, pp. 1289-1297. Prepublished online as a Blood First Edition Paper on October 5, 2006; DOI 10.1182/blood-2006-08-043364. This Article Full Text Full Text (PDF) Supplemental Videos All Versions of this Article: blood-2006-08-043364v1 109/3/1289    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Maier, A. G. Articles by Cowman, A. F. Search for Related Content PubMed PubMed Citation Articles by Maier, A. G. Articles by Cowman, A. F. Related Collections Red Cells Cytoskeleton Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  RED CELLS Skeleton-binding protein 1 functions at the parasitophorous vacuole membrane to traffic PfEMP1 to the Plasmodium falciparum–infected erythrocyte surface Alexander G. Maier1, Melanie Rug1, Matthew T. O'Neill1, James G. Beeson1, Matthias Marti1, John Reeder2, and Alan F. Cowman1 1 The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia; and 2 Papua New Guinea Institute of Medical Research, Goroka, Papua, New Guinea A key feature of Plasmodium falciparum, the parasite causing the most severe form of malaria in humans, is its ability to export parasite molecules onto the surface of the erythrocyte. The major virulence factor and variant surface protein PfEMP1 (P falciparum erythrocyte membrane protein 1) acts as a ligand to adhere to endothelial receptors avoiding splenic clearance. Because the erythrocyte is devoid of protein transport machinery, the parasite provides infrastructure for trafficking across membranes it traverses. In this study, we show that the P falciparum skeleton-binding protein 1 (PfSBP1) is required for transport of PfEMP1 to the P falciparum–infected erythrocyte surface. We present evidence that PfSBP1 functions at the parasitophorous vacuole membrane to load PfEMP1 into Maurer clefts during formation of these structures. Furthermore, the major reactivity of antibodies from malaria-exposed multigravid women is directed toward PfEMP1 because this is abolished in the absence of PfSBP1. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Bhattacharjee, C. van Ooij, B. Balu, J. H. Adams, and K. Haldar Maurer's clefts of Plasmodium falciparum are secretory organelles that concentrate virulence protein reporters for delivery to the host erythrocyte Blood, February 15, 2008; 111(4): 2418 - 2426. [Abstract] [Full Text] [PDF] S. R. Elliott, T. P. Spurck, J. M. Dodin, A. G. Maier, T. S. Voss, F. Yosaatmadja, P. D. Payne, G. I. McFadden, A. F. Cowman, S. J. Rogerson, et al. Inhibition of Dendritic Cell Maturation by Malaria Is Dose Dependent and Does Not Require Plasmodium falciparum Erythrocyte Membrane Protein 1 Infect. Immun., July 1, 2007; 75(7): 3621 - 3632. [Abstract] [Full Text] [PDF]

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