| http://purl.uniprot.org/citations/23975026 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23975026 | http://www.w3.org/2000/01/rdf-schema#comment | "Beta-cell dysfunction and impaired insulin production are hallmarks of diabetes, but despite the growing diabetes epidemic, the molecular mechanisms underlying this disease have remained unclear. We identified thioredoxin-interacting protein (TXNIP), a cellular redox regulator, as a crucial factor in beta-cell biology and show that beta-cell TXNIP is upregulated in diabetes, whereas TXNIP deficiency protects against diabetes by preventing beta-cell apoptosis. Here we show that TXNIP and diabetes induce beta-cell expression of a specific microRNA, miR-204, which in turn blocks insulin production by directly targeting and downregulating MAFA, a known insulin transcription factor. In particular, we first discovered the regulation of miR-204 by TXNIP by microarray analysis, followed by validation studies in INS-1 beta cells, islets of Txnip-deficient mice, diabetic mouse models and primary human islets. We then further found that TXNIP induces miR-204 by inhibiting the activity of signal transducer and activator of transcription 3 (STAT3), a transcription factor that is involved in miR-204 regulation. We also identified MAFA as a target that is downregulated by miR-204. Taken together, our results demonstrate that TXNIP controls microRNA expression and insulin production and that miR-204 is involved in beta-cell function. The newly identified TXNIP-miR-204-MAFA-insulin pathway may contribute to diabetes progression and provides new insight into TXNIP function and microRNA biology in health and disease."xsd:string |
| http://purl.uniprot.org/citations/23975026 | http://purl.org/dc/terms/identifier | "doi:10.1038/nm.3287"xsd:string |
| http://purl.uniprot.org/citations/23975026 | http://purl.uniprot.org/core/author | "Chen J."xsd:string |
| http://purl.uniprot.org/citations/23975026 | http://purl.uniprot.org/core/author | "Xu G."xsd:string |
| http://purl.uniprot.org/citations/23975026 | http://purl.uniprot.org/core/author | "Shalev A."xsd:string |
| http://purl.uniprot.org/citations/23975026 | http://purl.uniprot.org/core/author | "Jing G."xsd:string |
| http://purl.uniprot.org/citations/23975026 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23975026 | http://purl.uniprot.org/core/name | "Nat Med"xsd:string |
| http://purl.uniprot.org/citations/23975026 | http://purl.uniprot.org/core/pages | "1141-1146"xsd:string |
| http://purl.uniprot.org/citations/23975026 | http://purl.uniprot.org/core/title | "Thioredoxin-interacting protein regulates insulin transcription through microRNA-204."xsd:string |
| http://purl.uniprot.org/citations/23975026 | http://purl.uniprot.org/core/volume | "19"xsd:string |
| http://purl.uniprot.org/citations/23975026 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/23975026 |
| http://purl.uniprot.org/citations/23975026 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/23975026 |
| http://purl.uniprot.org/uniprot/#_Q8BG60-mappedCitation-23975026 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23975026 |
| http://purl.uniprot.org/uniprot/#_Q8CF90-mappedCitation-23975026 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23975026 |
| http://purl.uniprot.org/uniprot/#_Q91X82-mappedCitation-23975026 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23975026 |
| http://purl.uniprot.org/uniprot/Q91X82 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/23975026 |
| http://purl.uniprot.org/uniprot/Q8BG60 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/23975026 |
| http://purl.uniprot.org/uniprot/Q8CF90 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/23975026 |