| http://purl.uniprot.org/citations/22292036 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/22292036 | http://www.w3.org/2000/01/rdf-schema#comment | "The signaling pathways associated with the Toll-like receptors (TLRs) and nuclear factor-kappaB (NF-κB) are essential to pro-inflammatory cytokine and chemokine expression, as well as initiating innate epithelial immune responses. The TLR/NF-κB signaling pathways must be stringently controlled through an intricate network of positive and negative regulatory elements. MicroRNAs (miRNAs) are non-coding small RNAs that regulate the stability and/or translation of protein-coding mRNAs. Herein we report that miR-16 promotes NF-κB-regulated transactivation of the IL-8 gene by suppression of the silencing mediator for retinoid and thyroid hormone receptor (SMRT). LPS stimulation activated miR-16 gene transcription in human monocytes (U937) and biliary epithelial cells (H69) through MAPK-dependent mechanisms. Transfection of cells with the miR-16 precursor promoted LPS-induced production of IL-8, IL-6, and IL-1α, without a significant effect on their RNA stability. Instead, an increase in NF-κB-regulated transactivation of the IL-8 gene was confirmed in cells following transfection of miR-16 precursor. Importantly, miR-16 targeted the 3'-untranslated region of SMRT and caused translational suppression of SMRT. LPS decreased SMRT expression via upregulation of miR-16. Moreover, functional manipulation of SMRT altered NF-κB-regulated transactivation of LPS-induced IL-8 expression. These data suggest that miR-16 targets SMRT and modulates NF-κB-regulated transactivation of the IL-8 gene."xsd:string |
| http://purl.uniprot.org/citations/22292036 | http://purl.org/dc/terms/identifier | "doi:10.1371/journal.pone.0030772"xsd:string |
| http://purl.uniprot.org/citations/22292036 | http://purl.uniprot.org/core/author | "Hu G."xsd:string |
| http://purl.uniprot.org/citations/22292036 | http://purl.uniprot.org/core/author | "Li X."xsd:string |
| http://purl.uniprot.org/citations/22292036 | http://purl.uniprot.org/core/author | "Zhou R."xsd:string |
| http://purl.uniprot.org/citations/22292036 | http://purl.uniprot.org/core/author | "Chen X.M."xsd:string |
| http://purl.uniprot.org/citations/22292036 | http://purl.uniprot.org/core/author | "Drescher K.M."xsd:string |
| http://purl.uniprot.org/citations/22292036 | http://purl.uniprot.org/core/author | "Gong A.Y."xsd:string |
| http://purl.uniprot.org/citations/22292036 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/22292036 | http://purl.uniprot.org/core/name | "PLoS One"xsd:string |
| http://purl.uniprot.org/citations/22292036 | http://purl.uniprot.org/core/pages | "e30772"xsd:string |
| http://purl.uniprot.org/citations/22292036 | http://purl.uniprot.org/core/title | "miR-16 targets transcriptional corepressor SMRT and modulates NF-kappaB-regulated transactivation of interleukin-8 gene."xsd:string |
| http://purl.uniprot.org/citations/22292036 | http://purl.uniprot.org/core/volume | "7"xsd:string |
| http://purl.uniprot.org/citations/22292036 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/22292036 |
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