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http://purl.uniprot.org/citations/15226423http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15226423http://www.w3.org/2000/01/rdf-schema#comment"The human major histocompatibility complex (MHC) class Ib gene, HLA-E, codes for the major ligand of the inhibitory receptor NK-G-2A, which is present on most natural killer (NK) cells and some CD8(+) cytotoxic T lymphocytes. We have previously shown that gamma interferon (IFN-gamma) induction of HLA-E gene transcription is mediated through a distinct IFN-gamma-responsive element, the IFN response region (IRR), in all cell types studied. We have now identified and characterized a cell type-restricted enhancer of IFN-gamma-mediated induction of HLA-E gene transcription, designated the upstream interferon response region (UIRR), which is located immediately upstream of the IRR. The UIRR mediates a three-to eightfold enhancement of IFN-gamma induction of HLA-E transcription in some cell lines but not in others, and it functions only in the presence of an adjacent IRR. The UIRR contains a variant GATA binding site (AGATAC) that is critical to both IFN-gamma responsiveness and to the formation of a specific binding complex containing GATA-1 in K562 cell nuclear extracts. The binding of GATA-1 to this site in response to IFN-gamma was confirmed in vivo in a chromatin immunoprecipitation assay. Forced expression of GATA-1 in nonexpressing U937 cells resulted in a four-to fivefold enhancement of the IFN-gamma response from HLA-E promoter constructs containing a wild-type but not a GATA-1 mutant UIRR sequence and increased the IFN-gamma response of the endogenous HLA-E gene. Knockdown of GATA-1 expression in K562 cells resulted in a approximately 4-fold decrease in the IFN-gamma response of the endogenous HLA-E gene, consistent with loss of the increase in IFN-gamma response of HLA-E promoter-driven constructs containing the UIRR in wild-type K562 cells. Coexpression of wild-type and mutant adenovirus E1a proteins that sequester p300/CBP eliminated IFN-gamma-mediated enhancement through the UIRR, but only partially reduced induction through the IRR, implicating p300/CBP binding to Stat-1alpha at the IRR in the recruitment of GATA-1 to mediate the cooperation between the UIRR and IRR. We propose that the GATA-1 transcription factor represents a cell type-restricted mediator of IFN-gamma induction of the HLA-E gene."xsd:string
http://purl.uniprot.org/citations/15226423http://purl.org/dc/terms/identifier"doi:10.1128/mcb.24.14.6194-6204.2004"xsd:string
http://purl.uniprot.org/citations/15226423http://purl.uniprot.org/core/author"Wang J."xsd:string
http://purl.uniprot.org/citations/15226423http://purl.uniprot.org/core/author"Wang S.Z."xsd:string
http://purl.uniprot.org/citations/15226423http://purl.uniprot.org/core/author"Ginder G.D."xsd:string
http://purl.uniprot.org/citations/15226423http://purl.uniprot.org/core/author"Barrett D.M."xsd:string
http://purl.uniprot.org/citations/15226423http://purl.uniprot.org/core/author"Gustafson K.S."xsd:string
http://purl.uniprot.org/citations/15226423http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/15226423http://purl.uniprot.org/core/name"Mol Cell Biol"xsd:string
http://purl.uniprot.org/citations/15226423http://purl.uniprot.org/core/pages"6194-6204"xsd:string
http://purl.uniprot.org/citations/15226423http://purl.uniprot.org/core/title"A GATA factor mediates cell type-restricted induction of HLA-E gene transcription by gamma interferon."xsd:string
http://purl.uniprot.org/citations/15226423http://purl.uniprot.org/core/volume"24"xsd:string
http://purl.uniprot.org/citations/15226423http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/15226423
http://purl.uniprot.org/citations/15226423http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/15226423
http://purl.uniprot.org/uniprot/#_A0A0F7WBW2-mappedCitation-15226423http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15226423
http://purl.uniprot.org/uniprot/#_A0A0A8LFF7-mappedCitation-15226423http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15226423
http://purl.uniprot.org/uniprot/#_A0A0F7W1Q1-mappedCitation-15226423http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15226423
http://purl.uniprot.org/uniprot/#_P13747-mappedCitation-15226423http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15226423
http://purl.uniprot.org/uniprot/#_A0A7L7TM74-mappedCitation-15226423http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15226423
http://purl.uniprot.org/uniprot/#_A0A4E9DQ67-mappedCitation-15226423http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15226423
http://purl.uniprot.org/uniprot/#_A0A4E9E4P1-mappedCitation-15226423http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15226423
http://purl.uniprot.org/uniprot/#_A0A4E9E9K8-mappedCitation-15226423http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15226423
http://purl.uniprot.org/uniprot/#_B7WNQ9-mappedCitation-15226423http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15226423
http://purl.uniprot.org/uniprot/#_A0A4E9D3W4-mappedCitation-15226423http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15226423