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http://purl.uniprot.org/citations/23185455http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23185455http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23185455http://www.w3.org/2000/01/rdf-schema#comment"IL-2 plays a key role in the survival and proliferation of immune cells, especially T lymphocytes. Its expression is precisely regulated at transcriptional and posttranscriptional level. IL-2 is known to be regulated by RNA binding proteins, such as tristetraprolin (TTP), via an AU-rich element (ARE) in the 3'-untranslated region (3'UTR) to influence the stability of mRNA. MCPIP1, identified as a novel RNase, can degrade IL-6, IL-12 and TNF-α mRNA by an ARE-independent pathway in the activation of macrophages. Here, we reported that MCPIP1 was induced in the activation of T lymphocytes and negatively regulated IL-2 gene expression in both mouse and human primary T lymphocytes through destabilizing its mRNA. A set of Luciferase reporter assay demonstrated that a non-ARE conserved element in IL-2 3'UTR, which formed a stem-loop structure, responded to MCPIP1 activity.RNA immunoprecipitation and Biotin pulldown experiments further suggested that MCPIP1 could modestly bind to IL-2 mRNA. Taken together, these data demonstrate that MCPIP1 down-regulates IL-2 via an ARE-independent pathway."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0049841"xsd:string
http://purl.uniprot.org/citations/23185455http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0049841"xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Cai Z."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Cai Z."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Guo J."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Guo J."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Liu H."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Liu H."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Liu X."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Liu X."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Li M."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Li M."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Zhang W."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Zhang W."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Wang L."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Wang L."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Wang X."xsd:string
http://purl.uniprot.org/citations/23185455http://purl.uniprot.org/core/author"Wang X."xsd:string