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Malarial proteases and host cell egress: an ‘emerging’ cascade
Article first published online: 28 JUN 2008
© 2008 Medical Research Council (UK). Journal compilation © 2008 Blackwell Publishing Ltd
Volume 10, Issue 10, pages 1925–1934, October 2008
How to Cite
Blackman, M. J. (2008), Malarial proteases and host cell egress: an ‘emerging’ cascade. Cellular Microbiology, 10: 1925–1934. doi: 10.1111/j.1462-5822.2008.01176.x
- Issue published online: 8 SEP 2008
- Article first published online: 28 JUN 2008
- Received 4 April, 2008; revised 14 May, 2008; accepted 15 May, 2008.
Malaria is a scourge of large swathes of the globe, stressing the need for a continuing effort to better understand the biology of its aetiological agent. Like all pathogens of the phylum Apicomplexa, the malaria parasite spends part of its life inside a host cell or cyst. It eventually needs to escape (egress) from this protective environment to progress through its life cycle. Egress of Plasmodium blood-stage merozoites, liver-stage merozoites and mosquito midgut sporozoites relies on protease activity, so the enzymes involved have potential as antimalarial drug targets. This review examines the role of parasite proteases in egress, in the light of current knowledge of the mechanics of the process. Proteases implicated in egress include the cytoskeleton-degrading malarial proteases falcipain-2 and plasmepsin II, plus a family of putative papain-like proteases called SERA. Recent revelations have shown that activation of the SERA proteases may be triggered by regulated secretion of a subtilisin-like serine protease called SUB1. These findings are discussed in the context of the potential for development of new chemotherapeutics targeting this stage in the parasite's life cycle.