an erythrocyte vesicle protein exported by the malaria parasite promotes tubovesicular lipid import from the host cell surface疟原虫的红细胞泡蛋白出口促进tubovesicular脂质导入宿主细胞表面.pdfVIP
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an erythrocyte vesicle protein exported by the malaria parasite promotes tubovesicular lipid import from the host cell surface疟原虫的红细胞泡蛋白出口促进tubovesicular脂质导入宿主细胞表面
An Erythrocyte Vesicle Protein Exported by the Malaria
Parasite Promotes Tubovesicular Lipid Import from the
Host Cell Surface
1,2 1,2 1,2 3 ´ 4
Pamela A. Tamez , Souvik Bhattacharjee , Christiaan van Ooij , N. Luisa Hiller , Manuel Llinas ,
Bharath Balu5¤, John H. Adams5¤, Kasturi Haldar1,2*
1 Department of Pathology, Feinberg School of Medicine, Northwestern University Chicago, Illinois, United States of America, 2 Department of Microbiology-Immunology,
Feinberg School of Medicine, Northwestern University Chicago, Illinois, United States of America, 3 Allegheny General Hospital, Allegheny-Singer Research Institute,
Center for Genomic Sciences, Pittsburgh, Pennsylvania, United States of America, 4 Department of Molecular Biology, Lewis-Sigler Institute for Integrative Genomics,
Princeton University, Princeton, New Jersey, United States of America, 5 Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana, United States
of America
Abstract
Plasmodium falciparum is the protozoan parasite that causes the most virulent of human malarias. The blood stage parasites
export several hundred proteins into their host erythrocyte that underlie modifications linked to major pathologies of the
disease and parasite survival in the blood. Unfortunately, most are ‘hypothetical’ proteins of unknown function, and those
that are essential for parasitization of the erythrocyte cannot be ‘knocked out’. Here, we combined bioinformatics and
genome-wide expression analyses with a new series of transgenic and cellular assays to show for the first time in malaria
parasites that microarray read out from a chemical perturbation can have predictive value. W
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