| http://purl.uniprot.org/citations/23017470 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23017470 | http://www.w3.org/2000/01/rdf-schema#comment | "11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1, gene HSD11B1) converts glucocorticoid receptor-inert cortisone to receptor-active cortisol. Multiple evidence supports a causal role for 11β-HSD1 in the current obesity epidemic. In obese, HSD11B1 expression is increased in adipose tissue but typically decreased in liver, and the underlying tissue-specific mechanisms are largely unknown. In this context, we investigated a potential role of microRNAs (miRNAs). We used several miRNA target prediction tools to identify possible candidates and a publicly available miRNA expression atlas to further select candidates expressed in hepatocytes. Using a dual luciferase reporter assay, we identified three potential miRNAs, hsa-miR-340, -561 and -579, as potential negative regulators of HSD11B1 expression. Disruption of the corresponding microRNA response elements abolished repression of luciferase activity for hsa-miR-561 and -579, but not for hsa-miR-340. Furthermore, levels of firefly luciferase mRNA were not changed by miR-561 and -579, indicating a mechanism based on translational repression rather than mRNA degradation. Finally, we were able to detect both, miR-561 and -579, in human total liver RNA by reverse-transcription-polymerase chain reaction (RT-PCR). According to the presented results, miR-561 and -579 are likely to be involved in the tissue-specific regulation of HSD11B1 expression. Moreover, literature findings and a pathway enrichment analysis support a potential role of these two miRNAs in glucocorticoid metabolism and signalling and associated diseases."xsd:string |
| http://purl.uniprot.org/citations/23017470 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.jsbmb.2012.09.005"xsd:string |
| http://purl.uniprot.org/citations/23017470 | http://purl.uniprot.org/core/author | "Han Y."xsd:string |
| http://purl.uniprot.org/citations/23017470 | http://purl.uniprot.org/core/author | "Maser E."xsd:string |
| http://purl.uniprot.org/citations/23017470 | http://purl.uniprot.org/core/author | "Xiong G."xsd:string |
| http://purl.uniprot.org/citations/23017470 | http://purl.uniprot.org/core/author | "Staab-Weijnitz C.A."xsd:string |
| http://purl.uniprot.org/citations/23017470 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23017470 | http://purl.uniprot.org/core/name | "J Steroid Biochem Mol Biol"xsd:string |
| http://purl.uniprot.org/citations/23017470 | http://purl.uniprot.org/core/pages | "129-139"xsd:string |
| http://purl.uniprot.org/citations/23017470 | http://purl.uniprot.org/core/title | "Identification of microRNAs as a potential novel regulatory mechanism in HSD11B1 expression."xsd:string |
| http://purl.uniprot.org/citations/23017470 | http://purl.uniprot.org/core/volume | "133"xsd:string |
| http://purl.uniprot.org/citations/23017470 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/23017470 |
| http://purl.uniprot.org/citations/23017470 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/23017470 |
| http://purl.uniprot.org/uniprot/#_P28845-mappedCitation-23017470 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23017470 |
| http://purl.uniprot.org/uniprot/#_X5D2L1-mappedCitation-23017470 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23017470 |
| http://purl.uniprot.org/uniprot/P28845 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/23017470 |
| http://purl.uniprot.org/uniprot/X5D2L1 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/23017470 |