PubMed:26269592 JSONTXT

{"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":81},"obj":"Sentence"},{"id":"T2","span":{"begin":82,"end":237},"obj":"Sentence"},{"id":"T3","span":{"begin":238,"end":323},"obj":"Sentence"},{"id":"T4","span":{"begin":324,"end":418},"obj":"Sentence"},{"id":"T5","span":{"begin":419,"end":514},"obj":"Sentence"},{"id":"T6","span":{"begin":515,"end":591},"obj":"Sentence"},{"id":"T7","span":{"begin":592,"end":746},"obj":"Sentence"},{"id":"T8","span":{"begin":747,"end":878},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":81},"obj":"Sentence"},{"id":"T2","span":{"begin":82,"end":237},"obj":"Sentence"},{"id":"T3","span":{"begin":238,"end":323},"obj":"Sentence"},{"id":"T4","span":{"begin":324,"end":418},"obj":"Sentence"},{"id":"T5","span":{"begin":419,"end":514},"obj":"Sentence"},{"id":"T6","span":{"begin":515,"end":591},"obj":"Sentence"},{"id":"T7","span":{"begin":592,"end":746},"obj":"Sentence"},{"id":"T8","span":{"begin":747,"end":878},"obj":"Sentence"}],"text":"Signal Transduction and Intracellular Trafficking by the Interleukin 36 Receptor.\nImproper signaling of the IL-36 receptor (IL-36R), a member of the IL-1 receptor family, has been associated with various inflammation-associated diseases. However, the requirements for IL-36R signal transduction remain poorly characterized. This work seeks to define the requirements for IL-36R signaling and intracellular trafficking. In the absence of cognate agonists, IL-36R was endocytosed and recycled to the plasma membrane. In the presence of IL-36, IL-36R increased accumulation in LAMP1+ lysosomes. Endocytosis predominantly used a clathrin-mediated pathway, and the accumulation of the IL-36R in lysosomes did not result in increased receptor turnover. The ubiquitin-binding Tollip protein contributed to IL-36R signaling and increased the accumulation of both subunits of the IL-36R."}

{"project":"sentences","denotations":[{"id":"T1","span":{"begin":0,"end":81},"obj":"Sentence"},{"id":"T2","span":{"begin":82,"end":237},"obj":"Sentence"},{"id":"T3","span":{"begin":238,"end":323},"obj":"Sentence"},{"id":"T4","span":{"begin":324,"end":418},"obj":"Sentence"},{"id":"T5","span":{"begin":419,"end":514},"obj":"Sentence"},{"id":"T6","span":{"begin":515,"end":591},"obj":"Sentence"},{"id":"T7","span":{"begin":592,"end":746},"obj":"Sentence"},{"id":"T8","span":{"begin":747,"end":878},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Signal Transduction and Intracellular Trafficking by the Interleukin 36 Receptor.\nImproper signaling of the IL-36 receptor (IL-36R), a member of the IL-1 receptor family, has been associated with various inflammation-associated diseases. However, the requirements for IL-36R signal transduction remain poorly characterized. This work seeks to define the requirements for IL-36R signaling and intracellular trafficking. In the absence of cognate agonists, IL-36R was endocytosed and recycled to the plasma membrane. In the presence of IL-36, IL-36R increased accumulation in LAMP1+ lysosomes. Endocytosis predominantly used a clathrin-mediated pathway, and the accumulation of the IL-36R in lysosomes did not result in increased receptor turnover. The ubiquitin-binding Tollip protein contributed to IL-36R signaling and increased the accumulation of both subunits of the IL-36R."}

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":204,"end":216},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"}],"text":"Signal Transduction and Intracellular Trafficking by the Interleukin 36 Receptor.\nImproper signaling of the IL-36 receptor (IL-36R), a member of the IL-1 receptor family, has been associated with various inflammation-associated diseases. However, the requirements for IL-36R signal transduction remain poorly characterized. This work seeks to define the requirements for IL-36R signaling and intracellular trafficking. In the absence of cognate agonists, IL-36R was endocytosed and recycled to the plasma membrane. In the presence of IL-36, IL-36R increased accumulation in LAMP1+ lysosomes. Endocytosis predominantly used a clathrin-mediated pathway, and the accumulation of the IL-36R in lysosomes did not result in increased receptor turnover. The ubiquitin-binding Tollip protein contributed to IL-36R signaling and increased the accumulation of both subunits of the IL-36R."}

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":24,"end":37},"obj":"Body_part"},{"id":"T2","span":{"begin":392,"end":405},"obj":"Body_part"},{"id":"T3","span":{"begin":498,"end":513},"obj":"Body_part"},{"id":"T4","span":{"begin":581,"end":590},"obj":"Body_part"},{"id":"T5","span":{"begin":690,"end":699},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/GO_0005622"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/GO_0005622"},{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/GO_0005886"},{"id":"A4","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/GO_0005764"},{"id":"A5","pred":"uberon_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/GO_0005764"}],"text":"Signal Transduction and Intracellular Trafficking by the Interleukin 36 Receptor.\nImproper signaling of the IL-36 receptor (IL-36R), a member of the IL-1 receptor family, has been associated with various inflammation-associated diseases. However, the requirements for IL-36R signal transduction remain poorly characterized. This work seeks to define the requirements for IL-36R signaling and intracellular trafficking. In the absence of cognate agonists, IL-36R was endocytosed and recycled to the plasma membrane. In the presence of IL-36, IL-36R increased accumulation in LAMP1+ lysosomes. Endocytosis predominantly used a clathrin-mediated pathway, and the accumulation of the IL-36R in lysosomes did not result in increased receptor turnover. The ubiquitin-binding Tollip protein contributed to IL-36R signaling and increased the accumulation of both subunits of the IL-36R."}