http://purl.uniprot.org/citations/9139687 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/9139687 | http://www.w3.org/2000/01/rdf-schema#comment | "E2F is a heterodimeric transcription factor that controls transcription of several growth-regulatory genes including cdc2. To investigate the mechanism of interferon-alpha (IFN-alpha)-mediated growth suppression of hematopoietic cells, we examined the effect of IFN-alpha on the expression and function of E2F using IFN-sensitive Daudi cells. Down-regulation of E2F-1, a subunit of E2F, was observed after 8 h of culture with IFN-alpha; expression of E2F-4, another subunit of E2F, and DP-1, a heterodimeric partner of E2F, was unaffected. Gel shift assays revealed that the DNA binding activity of free E2F, which is composed of E2F-1 and E2F-4, was inhibited by IFN-alpha. In contrast, IFN-alpha did not affect the DNA binding ability of E2F-1 and E2F-4 in a complex with retinoblastoma (RB) susceptibility gene family proteins including pRB, p107, and p130. IFN-alpha could induce dephosphorylation of pRB, thereby turning active E2F-pRB complexes into transcriptional repressors. Transient chloramphenicol acetyltransferase assays revealed that the activity of the E2F-dependent cdc2 promoter was suppressed by IFN-alpha. These results suggest that the antiproliferative action of IFN-alpha is mediated through the modulation of E2F activity in two different ways: down-regulation of transcriptionally active free E2F and conversion of E2F-pRB complexes into transcriptional repressors."xsd:string |
http://purl.uniprot.org/citations/9139687 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.272.19.12406"xsd:string |
http://purl.uniprot.org/citations/9139687 | http://purl.uniprot.org/core/author | "Kikuchi J."xsd:string |
http://purl.uniprot.org/citations/9139687 | http://purl.uniprot.org/core/author | "Nakamura M."xsd:string |
http://purl.uniprot.org/citations/9139687 | http://purl.uniprot.org/core/author | "Yamada H."xsd:string |
http://purl.uniprot.org/citations/9139687 | http://purl.uniprot.org/core/author | "Terui Y."xsd:string |
http://purl.uniprot.org/citations/9139687 | http://purl.uniprot.org/core/author | "Furukawa Y."xsd:string |
http://purl.uniprot.org/citations/9139687 | http://purl.uniprot.org/core/author | "Nagai M."xsd:string |
http://purl.uniprot.org/citations/9139687 | http://purl.uniprot.org/core/author | "Iwase S."xsd:string |
http://purl.uniprot.org/citations/9139687 | http://purl.uniprot.org/core/date | "1997"xsd:gYear |
http://purl.uniprot.org/citations/9139687 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
http://purl.uniprot.org/citations/9139687 | http://purl.uniprot.org/core/pages | "12406-12414"xsd:string |
http://purl.uniprot.org/citations/9139687 | http://purl.uniprot.org/core/title | "Modulation of E2F activity is linked to interferon-induced growth suppression of hematopoietic cells."xsd:string |
http://purl.uniprot.org/citations/9139687 | http://purl.uniprot.org/core/volume | "272"xsd:string |
http://purl.uniprot.org/citations/9139687 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/9139687 |
http://purl.uniprot.org/citations/9139687 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/9139687 |
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http://purl.uniprot.org/uniprot/#_Q3V3X3-mappedCitation-9139687 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/9139687 |
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