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http://purl.uniprot.org/citations/36593296http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/36593296http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/36593296http://www.w3.org/2000/01/rdf-schema#comment"Staphylococcus aureus invades cells and persists intracellularly, causing persistent inflammation that is notoriously difficult to treat. Here we investigated host-pathogen interactions underlying intracellular S. aureus infection in macrophages and discovered that the endoplasmic reticulum (ER) is an important cellular compartment for intracellular S. aureus infection. Using CRISPR-Cas9 guide RNA library screening, we determined that the autocrine motility factor receptor (AMFR), an ER-resident E3 ubiquitin ligase, played an essential role in mediating intracellular S. aureus-induced inflammation. AMFR directly interacted with TAK1-binding protein 3 (TAB3) in the ER, inducing K27-linked polyubiquitination of TAB3 on lysine 649 and promoting TAK1 activation. Moreover, the virulence factor γ-haemolysin B (HIgB) of S. aureus bound to the AMFR and regulated TAB3. Our findings highlight an unknown role of AMFR in intracellular S. aureus infection-induced pneumonia and suggest that pharmacological interruption of AMFR-mediated TAB3 signalling cascades and HIgB targeting may prevent invasive staphylococci-mediated pneumonia."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.org/dc/terms/identifier"doi:10.1038/s41564-022-01278-7"xsd:string
http://purl.uniprot.org/citations/36593296http://purl.org/dc/terms/identifier"doi:10.1038/s41564-022-01278-7"xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Chen D."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Chen D."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Lou X."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Lou X."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Wu Y."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Wu Y."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Sun L."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Sun L."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Yang X."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Yang X."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Wang Z."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Wang Z."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Zhang A."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Zhang A."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Guo B."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Guo B."xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Zhang H.'"xsd:string
http://purl.uniprot.org/citations/36593296http://purl.uniprot.org/core/author"Zhang H.'"xsd:string