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http://purl.uniprot.org/citations/25354317http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25354317http://www.w3.org/2000/01/rdf-schema#comment"β-Arrestins (β-arrs) are regulators and mediators of G protein-coupled receptor signaling, and accumulating evidence suggests that they are functionally involved in inflammation and autoimmune diseases. However, the effect of β-arrs is unclear in inflammatory bowel disease (IBD), and the role of β-arr2 is unknown in ulcerative colitis (UC) and Crohn's disease (CD). The aim of this study is to investigate whether β-arr2 encourages inflammation-induced epithelial apoptosis through endoplasmic reticulum (ER) stress/p53-upregulated modulator of apoptosis (PUMA) in colitis. In the present study, the results showed that β-arr2 was increased in specimens from patients with UC or CD. Furthermore, a β-arr2 deficiency significantly repressed intestinal inflammation, ameliorated colitis, and alleviated mucosal apoptosis in mice. In addition, the targeted deletion of β-arr2 depressed ER stress, inhibited PUMA, and downregulated PUMA-mediated mitochondrial apoptotic signaling in colitis. β-Arr2, an important modulator of G protein-coupled receptor function, binds eIF2α to activate ER stress signaling. Furthermore, the knockdown of PUMA dramatically prevented β-arr2-induced apoptosis via alleviating ER stress in vitro. The results suggest that β-arr2 encourages inflammation-induced epithelial apoptosis through ER stress/PUMA in colitis and that β-arr2 is a potential therapeutic target for colitis."xsd:string
http://purl.uniprot.org/citations/25354317http://purl.org/dc/terms/identifier"doi:10.1038/mi.2014.104"xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/author"Jiang J."xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/author"Tao J."xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/author"Wu B."xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/author"Liu H.L."xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/author"Liu Z.H."xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/author"Yang Y.D."xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/author"Tan S.W."xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/author"Peng X.J."xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/author"Zeng L.X."xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/name"Mucosal Immunol"xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/pages"683-695"xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/title"beta-Arrestin2 encourages inflammation-induced epithelial apoptosis through ER stress/PUMA in colitis."xsd:string
http://purl.uniprot.org/citations/25354317http://purl.uniprot.org/core/volume"8"xsd:string
http://purl.uniprot.org/citations/25354317http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25354317
http://purl.uniprot.org/citations/25354317http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25354317
http://purl.uniprot.org/uniprot/#_A0A158SIT9-mappedCitation-25354317http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25354317
http://purl.uniprot.org/uniprot/#_B2RVL4-mappedCitation-25354317http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25354317
http://purl.uniprot.org/uniprot/#_A8K4I6-mappedCitation-25354317http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25354317
http://purl.uniprot.org/uniprot/#_B4DQK3-mappedCitation-25354317http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25354317
http://purl.uniprot.org/uniprot/#_J3JS97-mappedCitation-25354317http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25354317
http://purl.uniprot.org/uniprot/#_K7ENA6-mappedCitation-25354317http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25354317