| http://purl.uniprot.org/citations/18771758 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18771758 | http://www.w3.org/2000/01/rdf-schema#comment | "Programmed death-1 (PD-1), an immunoinhibitory receptor, is upregulated in T cells, B cells, NKT cells, and monocytes upon activation. More specifically, T-cell-associated PD-1 is critically important for maintaining peripheral tolerance through the PD-1-B7-H1 pathway. However, the physiological role of macrophage-associated PD-1 remains unclear. We addressed the molecular mechanism underlying the regulation of PD-1 expression on macrophages in response to IFN-alpha. Based on a luciferase assay using promoter constructs, we found that the promoter region located between -1090 and -1105 nucleotides from the translational start site is essential for PD-1 expression. Electrophoretic mobility-shift assay and site-directed mutagenesis revealed that interferon-sensitive responsive element (ISRE) and STAT1 and STAT2 are primarily responsible for the constitutive expression of PD-1, as well as for the IFN-alpha-mediated upregulation of PD-1. In addition, AG490, a Janus-activated kinase/signal transducer and activator of transcription (JAK/STAT) inhibitor, markedly abolished the responsiveness of bone marrow-derived macrophages (BMM) to IFN-alpha. Our findings support the essential roles of ISRE, STAT1, and STAT2 in the regulation of constitutive and IFN-alpha-mediated PD-1 expression in macrophages."xsd:string |
| http://purl.uniprot.org/citations/18771758 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.bbagrm.2008.08.003"xsd:string |
| http://purl.uniprot.org/citations/18771758 | http://purl.uniprot.org/core/author | "Lee S.W."xsd:string |
| http://purl.uniprot.org/citations/18771758 | http://purl.uniprot.org/core/author | "Cho H.Y."xsd:string |
| http://purl.uniprot.org/citations/18771758 | http://purl.uniprot.org/core/author | "Choi I."xsd:string |
| http://purl.uniprot.org/citations/18771758 | http://purl.uniprot.org/core/author | "Seo S.K."xsd:string |
| http://purl.uniprot.org/citations/18771758 | http://purl.uniprot.org/core/author | "Lee S.W.'"xsd:string |
| http://purl.uniprot.org/citations/18771758 | http://purl.uniprot.org/core/author | "Choi I.W."xsd:string |
| http://purl.uniprot.org/citations/18771758 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18771758 | http://purl.uniprot.org/core/name | "Biochim Biophys Acta"xsd:string |
| http://purl.uniprot.org/citations/18771758 | http://purl.uniprot.org/core/pages | "811-819"xsd:string |
| http://purl.uniprot.org/citations/18771758 | http://purl.uniprot.org/core/title | "Interferon-sensitive response element (ISRE) is mainly responsible for IFN-alpha-induced upregulation of programmed death-1 (PD-1) in macrophages."xsd:string |
| http://purl.uniprot.org/citations/18771758 | http://purl.uniprot.org/core/volume | "1779"xsd:string |
| http://purl.uniprot.org/citations/18771758 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18771758 |
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