http://purl.uniprot.org/citations/23825189 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/23825189 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/23825189 | http://www.w3.org/2000/01/rdf-schema#comment | "Reversible ubiquitin modification of cell signaling molecules has emerged as a critical mechanism by which cells respond to extracellular stimuli. Although ubiquitination of TGF-β-activated kinase 1 (TAK1) is critical for NF-κB activation in T cells, the regulation of its deubiquitination is unclear. We show that USP18, which was previously reported to be important in regulating type I interferon signaling in innate immunity, regulates T cell activation and T helper 17 (Th17) cell differentiation by deubiquitinating the TAK1-TAB1 complex. USP18-deficient T cells are defective in Th17 differentiation and Usp18(-/-) mice are resistant to experimental autoimmune encephalomyelitis (EAE). In response to T cell receptor engagement, USP18-deficient T cells exhibit hyperactivation of NF-κB and NFAT and produce increased levels of IL-2 compared with the wild-type controls. Importantly, USP18 is associated with and deubiquitinates the TAK1-TAB1 complex, thereby restricting expression of IL-2. Our findings thus demonstrate a previously uncharacterized negative regulation of TAK1 activity during Th17 differentiation, suggesting that USP18 may be targeted to treat autoimmune diseases."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.org/dc/terms/identifier | "doi:10.1084/jem.20122327"xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.org/dc/terms/identifier | "doi:10.1084/jem.20122327"xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Li H."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Li H."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Liu X."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Liu X."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Lin X."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Lin X."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Zhong B."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Zhong B."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Yan M."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Yan M."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Dong C."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Dong C."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Zhang D.E."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Zhang D.E."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Tian Q."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Tian Q."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Gorjestani S."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Gorjestani S."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Blonska M."xsd:string |
http://purl.uniprot.org/citations/23825189 | http://purl.uniprot.org/core/author | "Blonska M."xsd:string |