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dc.contributor.authorGuidi, Cynthia J.
dc.contributor.authorVeal, Timothy M.
dc.contributor.authorJones, Stephen N.
dc.contributor.authorImbalzano, Anthony N.
dc.date2022-08-11T08:08:58.000
dc.date.accessioned2022-08-23T16:14:09Z
dc.date.available2022-08-23T16:14:09Z
dc.date.issued2004-02-06
dc.date.submitted2008-09-23
dc.identifier.citationJ Biol Chem. 2004 Feb 6;279(6):4180-5. Epub 2003 Nov 20. <a href="http://dx.doi.org/10.1074/jbc.M312043200">Link to article on publisher's site</a>
dc.identifier.issn0021-9258 (Print)
dc.identifier.doi10.1074/jbc.M312043200
dc.identifier.pmid14630919
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33793
dc.description.abstractThe gene encoding INI1, a component of the mammalian SWI/SNF ATP-dependent chromatin remodeling enzymes, has been classified as a tumor suppressor in humans. Gene-targeting experiments confirmed that Ini1 also functions as a tumor suppressor in mice. Although Ini1-null mice are embryonic lethal, 15-30% of mice heterozygous for Ini1 presented with poorly differentiated tumors with variable rhabdoid features. All tumors examined showed loss of heterozygosity at the Ini1 locus. We report here that cells and tissues heterozygous for the Ini1 tumor suppressor express levels of Ini1 protein and message roughly equivalent to the levels observed in wild type counterparts. Compensation of Ini1 is mediated by an increase in the rate of transcription from the Ini1 promoter. Moreover, when Ini1 is expressed exogenously, transcription from the endogenous promoter is reduced, suggesting that Ini1 levels are tightly regulated. This is the first report describing transcriptional compensation for haploinsufficiency of a tumor suppressor gene.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14630919&dopt=Abstract">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1074/jbc.M312043200
dc.subjectAlleles; Animals; Base Sequence; Cells, Cultured; Chromosomal Proteins, Non-Histone; DNA-Binding Proteins; *Genes, Tumor Suppressor; Heterozygote; Mice; Mice, Mutant Strains; Neoplasms, Experimental; Promoter Regions (Genetics); RNA, Messenger; Transcription, Genetic
dc.subjectCell Biology
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleTranscriptional compensation for loss of an allele of the Ini1 tumor suppressor
dc.typeJournal Article
dc.source.journaltitleThe Journal of biological chemistry
dc.source.volume279
dc.source.issue6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/455
dc.identifier.contextkey635950
html.description.abstract<p>The gene encoding INI1, a component of the mammalian SWI/SNF ATP-dependent chromatin remodeling enzymes, has been classified as a tumor suppressor in humans. Gene-targeting experiments confirmed that Ini1 also functions as a tumor suppressor in mice. Although Ini1-null mice are embryonic lethal, 15-30% of mice heterozygous for Ini1 presented with poorly differentiated tumors with variable rhabdoid features. All tumors examined showed loss of heterozygosity at the Ini1 locus. We report here that cells and tissues heterozygous for the Ini1 tumor suppressor express levels of Ini1 protein and message roughly equivalent to the levels observed in wild type counterparts. Compensation of Ini1 is mediated by an increase in the rate of transcription from the Ini1 promoter. Moreover, when Ini1 is expressed exogenously, transcription from the endogenous promoter is reduced, suggesting that Ini1 levels are tightly regulated. This is the first report describing transcriptional compensation for haploinsufficiency of a tumor suppressor gene.</p>
dc.identifier.submissionpathgsbs_sp/455
dc.contributor.departmentDepartment of Cell Biology
dc.source.pages4180-5
dc.contributor.studentCynthia J. Guidi


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