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dc.contributor.authorMontecino, Martin A.
dc.contributor.authorStein, Janet L.
dc.contributor.authorStein, Gary S.
dc.contributor.authorLian, Jane B.
dc.contributor.authorVan Wijnen, Andre J.
dc.contributor.authorCruzat, Fernando
dc.contributor.authorGutierrez, Soraya E.
dc.contributor.authorOlate, Juan
dc.contributor.authorMarcellini, Sylvain
dc.contributor.authorGutierrez, Jose L.
dc.date2022-08-11T08:08:58.000
dc.date.accessioned2022-08-23T16:14:07Z
dc.date.available2022-08-23T16:14:07Z
dc.date.issued2007-08-24
dc.date.submitted2008-09-22
dc.identifier.citationBiochem Cell Biol. 2007 Aug;85(4):419-25. <a href="http://dx.doi.org/10.1139/o07-070">Link to article on publisher's site</a>
dc.identifier.issn0829-8211 (Print)
dc.identifier.doi10.1139/o07-070
dc.identifier.pmid17713577
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33784
dc.description.abstractChromatin organization within the nuclear compartment is a fundamental mechanism to regulate the expression of eukaryotic genes. During the last decade, a number of nuclear protein complexes with the ability to remodel chromatin and regulate gene transcription have been reported. Among these complexes is the SWI/SNF family, which alters chromatin structure in an ATP-dependent manner. A considerable effort has been made to understand the molecular mechanisms by which SWI/SNF catalyzes nucleosome remodeling. However, limited attention has been dedicated to studying the role of the DNA sequence in this remodeling process. Therefore, in this minireview, we discuss the contribution of nucleosome positioning and nucleosome excluding sequences to the targeting and activity of SWI/SNF complexes. This discussion includes results from our group using the rat osteocalcin gene promoter as a model. Based on these results, we postulate a model for chromatin remodeling and transcriptional activation of this gene in osteoblastic cells.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17713577&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1139/o07-070
dc.subjectAnimals; *Base Sequence; *Chromatin Assembly and Disassembly; Chromosomal Proteins, Non-Histone; *DNA; Models, Genetic; *Nucleosomes; Osteocalcin; Promoter Regions (Genetics); Transcription Factors; Transcription, Genetic
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleNucleosome organization and targeting of SWI/SNF chromatin-remodeling complexes: contributions of the DNA sequence
dc.typeJournal Article
dc.source.journaltitleBiochemistry and cell biology = Biochimie et biologie cellulaire
dc.source.volume85
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/446
dc.identifier.contextkey635321
html.description.abstract<p>Chromatin organization within the nuclear compartment is a fundamental mechanism to regulate the expression of eukaryotic genes. During the last decade, a number of nuclear protein complexes with the ability to remodel chromatin and regulate gene transcription have been reported. Among these complexes is the SWI/SNF family, which alters chromatin structure in an ATP-dependent manner. A considerable effort has been made to understand the molecular mechanisms by which SWI/SNF catalyzes nucleosome remodeling. However, limited attention has been dedicated to studying the role of the DNA sequence in this remodeling process. Therefore, in this minireview, we discuss the contribution of nucleosome positioning and nucleosome excluding sequences to the targeting and activity of SWI/SNF complexes. This discussion includes results from our group using the rat osteocalcin gene promoter as a model. Based on these results, we postulate a model for chromatin remodeling and transcriptional activation of this gene in osteoblastic cells.</p>
dc.identifier.submissionpathgsbs_sp/446
dc.contributor.departmentDepartment of Cell Biology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages419-25


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