RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/19164764http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19164764http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19164764http://www.w3.org/2000/01/rdf-schema#comment"Gfi-1 is a nuclear zinc finger (ZF) transcriptional repressor that plays an important role in hematopoiesis and inner ear development, and has been implicated in lymphomagenesis. Gfi-1 represses transcription by directly binding to the consensus DNA sequence in the promoters of its target genes. We report here an alternative mechanism by which Gfi-1 represses CDKN2B encoding p15(INK4B). Gfi-1 does not directly bind to CDKN2B, but interacts with Miz-1 and, via Miz-1, is recruited to the core promoter of CDKN2B. Miz-1 is a POZ-ZF transcription factor that has been shown to mediate transcriptional repression by c-Myc. Like c-Myc, upon recruitment to the CDKN2B promoter, Gfi-1 represses transcriptional activation of CDKN2B by Miz-1 and in response to TGFbeta. Consistent with its role in repressing CDKN2B transcription, knockdown of Gfi-1 in human leukemic cells or deficiency of Gfi-1 in mouse bone marrow cells results in augmented expression of p15(INK4B). Notably, Gfi-1 and c-Myc are both recruited to the CDKN2B core promoter and act in collaboration to repress CDKN2B. Our data reveal a mechanism of transcriptional repression by Gfi-1 and may have important implications for understanding the roles of Gfi-1 in normal development and tumorigenesis."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0804863106"xsd:string
http://purl.uniprot.org/citations/19164764http://purl.org/dc/terms/identifier"doi:10.1073/pnas.0804863106"xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/author"Liu Q."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/author"Liu Q."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/author"Dong F."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/author"Dong F."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/author"Qiu Y."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/author"Qiu Y."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/author"Basu S."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/author"Basu S."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/name"Proc. Natl. Acad. Sci. U.S.A."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/name"Proc. Natl. Acad. Sci. U.S.A."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/pages"1433-1438"xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/pages"1433-1438"xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/title"Gfi-1 represses CDKN2B encoding p15INK4B through interaction with Miz-1."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/title"Gfi-1 represses CDKN2B encoding p15INK4B through interaction with Miz-1."xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/volume"106"xsd:string
http://purl.uniprot.org/citations/19164764http://purl.uniprot.org/core/volume"106"xsd:string
http://purl.uniprot.org/citations/19164764http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19164764
http://purl.uniprot.org/citations/19164764http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19164764