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dc.contributor.authorHill, David A.
dc.contributor.authorImbalzano, Anthony N.
dc.date2022-08-11T08:09:08.000
dc.date.accessioned2022-08-23T16:18:40Z
dc.date.available2022-08-23T16:18:40Z
dc.date.issued2006-02-03
dc.date.submitted2011-02-09
dc.identifier.citationGene. 2006 Apr 12;371(1):59-67. Epub 2006 Jan 31. <a href="http://dx.doi.org/10.1016/j.gene.2005.11.012">Link to article on publisher's site</a>
dc.identifier.issn0378-1119 (Linking)
dc.identifier.doi10.1016/j.gene.2005.11.012
dc.identifier.pmid16451822
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34867
dc.description.abstractExpression of key regulatory and tissue specific proteins necessary for myogenesis and adipogenesis are dependent on functional SWI/SNF enzymes that hydrolyze ATP to remodel chromatin and allow factors access to chromatinized DNA. Functional chromatin structural changes also can be facilitated by the high mobility group-N1 (HMGN1) protein. HMGN1 is a chromatin architectural protein that specifically interacts with nucleosomes and has been shown to facilitate the reversal of repressive chromatin structure, thereby making it more conducive for transcription. To determine if HMGN1 functions in myogenesis or adipogensis, two SWI/SNF-dependent processes, we used RNA interference to created stable cell lines with reduced HMGN1 protein levels and differentiated them along the myogenic and adipogenic pathways. We show that neither myogenesis nor adipogenesis was affected by reduced HMGN1 protein levels. We further demonstrate that HMGN1 levels naturally decrease as a function of contact-mediated cell cycle arrest, thereby explaining the lack of requirement for HMGN1 in these cellular differentiation processes.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=16451822&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.gene.2005.11.012
dc.subjectAdipogenesis
dc.subjectAnimals
dc.subjectCell Cycle
dc.subjectCell Differentiation
dc.subjectChromatin Assembly and Disassembly
dc.subjectHMGN1 Protein
dc.subjectMice
dc.subjectMuscle Development
dc.subjectNIH 3T3 Cells
dc.subjectNucleosomes
dc.subjectRNA Interference
dc.subjectCell Biology
dc.titleHMGN1 is dispensable for myogenesis and adipogenesis
dc.typeJournal Article
dc.source.journaltitleGene
dc.source.volume371
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/imbalzano/8
dc.identifier.contextkey1773784
html.description.abstract<p>Expression of key regulatory and tissue specific proteins necessary for myogenesis and adipogenesis are dependent on functional SWI/SNF enzymes that hydrolyze ATP to remodel chromatin and allow factors access to chromatinized DNA. Functional chromatin structural changes also can be facilitated by the high mobility group-N1 (HMGN1) protein. HMGN1 is a chromatin architectural protein that specifically interacts with nucleosomes and has been shown to facilitate the reversal of repressive chromatin structure, thereby making it more conducive for transcription. To determine if HMGN1 functions in myogenesis or adipogensis, two SWI/SNF-dependent processes, we used RNA interference to created stable cell lines with reduced HMGN1 protein levels and differentiated them along the myogenic and adipogenic pathways. We show that neither myogenesis nor adipogenesis was affected by reduced HMGN1 protein levels. We further demonstrate that HMGN1 levels naturally decrease as a function of contact-mediated cell cycle arrest, thereby explaining the lack of requirement for HMGN1 in these cellular differentiation processes.</p>
dc.identifier.submissionpathimbalzano/8
dc.contributor.departmentDepartment of Cell Biology
dc.source.pages59-67


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