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NOT Open Access | An exported kinase family mediates species-specific erythrocyte remodelling and virulence in human malaria

April 15, 2020 - 14:15 -- NOT Open Access
Davies H, Belda H, Broncel M, Ye X, Bisson C, Introini V, Dorin-Semblat D, Semblat JP, Tibúrcio M, Gamain B, Kaforou M, Treeck M
Nat Microbiol. 2020 Apr 13. doi: 10.1038/s41564-020-0702-4

The most severe form of human malaria is caused by Plasmodium falciparum. Its virulence is closely linked to the increase in rigidity of infected erythrocytes and their adhesion to endothelial receptors, obstructing blood flow to vital organs. Unlike other human-infecting Plasmodium species, P. falciparum exports a family of 18 FIKK serine/threonine kinases into the host cell, suggesting that phosphorylation may modulate erythrocyte modifications.

A novel Plasmodium yoelii pseudokinase, PypPK1, is involved in erythrocyte invasion and exflagellation center formation

January 27, 2020 - 13:22 -- Open Access
Ishizaki T, Chaiyawong N, Hakimi H, Asada M, Tachibana M, Ishino T, Yahata K, Kaneko O
Parasitology International, 14 January 2020, 102056

Malaria parasites proliferate by repeated invasion of and multiplication within erythrocytes in the vertebrate host. Sexually committed intraerythrocytic parasites undergo sexual stage differentiation to become gametocytes. After ingestion by the mosquito, male and female gametocytes egress from erythrocytes and fertilize within the mosquito midgut. A complex signaling pathway likely responds to environmental events to trigger gametogenesis and regulate fertilization; however, such knowledge remains limited for malaria parasites.


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