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pubmed-article:18243132pubmed:abstractTextImitation Switch (ISWI) is a member of the SWI2/SNF2 superfamily of ATP-dependent chromatin remodelers, which are involved in multiple nuclear functions, including transcriptional regulation, replication, and chromatin assembly. Mammalian genomes encode two ISWI orthologs, SNF2H and SNF2L. In order to clarify the molecular mechanisms governing the expression of human SNF2L gene, we functionally examined the transcriptional regulation of human SNF2L promoter. Reporter gene assays demonstrated that the minimal SNF2L promoter was located between positions -152 to -86 relative to the transcription start site. In this region we have identified a cAMP-response element (CRE) located at -99 to -92 and a Sp1-binding site at -145 to -135 that play a critical role in regulating basal activity of human SNF2L gene, which were proven by deletion and mutation of specific binding sites, EMSA, and down-regulating Sp1 and CREB via RNAi. This study provides the first insight into the mechanisms that control basal expression of human SNF2L gene.lld:pubmed
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pubmed-article:18243132pubmed:pagination438-44lld:pubmed
pubmed-article:18243132pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:18243132pubmed:articleTitleSp1 and CREB regulate basal transcription of the human SNF2L gene.lld:pubmed
pubmed-article:18243132pubmed:affiliationKey Laboratory for Experimental Teratology of the Ministry of Education and Institute of Medical Genetics, Shandong University School of Medicine, Jinan, Shandong 250012, China.lld:pubmed
pubmed-article:18243132pubmed:publicationTypeJournal Articlelld:pubmed
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