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http://purl.uniprot.org/citations/29109477http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29109477http://www.w3.org/2000/01/rdf-schema#comment"The causative agent of malaria, Plasmodium, replicates inside a membrane-bound parasitophorous vacuole (PV), which shields this intracellular parasite from the cytosol of the host cell 1 . One common threat for intracellular pathogens is the homeostatic process of autophagy, through which cells capture unwanted intracellular material for lysosomal degradation 2 . During the liver stage of a malaria infection, Plasmodium parasites are targeted by the autophagy machinery of the host cell, and the PV membrane (PVM) becomes decorated with several autophagy markers, including LC3 (microtubule-associated protein 1 light chain 3) 3,4 . Here we show that Plasmodium berghei parasites infecting hepatic cells rely on the PVM transmembrane protein UIS3 to avoid elimination by host-cell-mediated autophagy. We found that UIS3 binds host LC3 through a non-canonical interaction with a specialized surface on LC3 where host proteins with essential functions during autophagy also bind. UIS3 acts as a bona fide autophagy inhibitor by competing with host LC3-interacting proteins for LC3 binding. Our work identifies UIS3, one of the most promising candidates for a genetically attenuated vaccine against malaria 5 , as a unique and potent mediator of autophagy evasion in Plasmodium. We propose that the protein-protein interaction between UIS3 and host LC3 represents a target for antimalarial drug development."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.org/dc/terms/identifier"doi:10.1038/s41564-017-0054-x"xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/author"Mair G.R."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/author"Mota M.M."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/author"Enguita F.J."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/author"Rodrigues L."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/author"Beatty W."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/author"Mancio-Silva L."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/author"Real E."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/author"Cabal G.G."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/author"Figueira T.N."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/author"Zuzarte-Luis V."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/author"Mello-Vieira J."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/author"Vera I.M."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/name"Nat Microbiol"xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/pages"17-25"xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/title"Plasmodium UIS3 sequesters host LC3 to avoid elimination by autophagy in hepatocytes."xsd:string
http://purl.uniprot.org/citations/29109477http://purl.uniprot.org/core/volume"3"xsd:string
http://purl.uniprot.org/citations/29109477http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29109477
http://purl.uniprot.org/citations/29109477http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29109477
http://purl.uniprot.org/uniprot/#_Q91VR7-mappedCitation-29109477http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29109477
http://purl.uniprot.org/uniprot/Q91VR7http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/29109477