Snf5 tumor suppressor couples chromatin remodeling, checkpoint control, and chromosomal stability
| dc.contributor.author | Imbalzano, Anthony N. | |
| dc.contributor.author | Jones, Stephen N. | |
| dc.date | 2022-08-11T08:09:15.000 | |
| dc.date.accessioned | 2022-08-23T16:23:58Z | |
| dc.date.available | 2022-08-23T16:23:58Z | |
| dc.date.issued | 2005-04-20 | |
| dc.date.submitted | 2011-01-28 | |
| dc.identifier.citation | Cancer Cell. 2005 Apr;7(4):294-5. <a href="http://dx.doi.org/10.1016/j.ccr.2005.04.001">Link to article on publisher's site</a> | |
| dc.identifier.issn | 1535-6108 (Linking) | |
| dc.identifier.doi | 10.1016/j.ccr.2005.04.001 | |
| dc.identifier.uri | http://hdl.handle.net/20.500.14038/36018 | |
| dc.description.abstract | SNF5 is a core subunit of the SWI/SNF chromatin-remodeling complex. Mammalian SNF5 is essential for normal cell viability, and loss or mutation of the human SNF gene is the molecular basis for familial malignant rhabdoid tumorigenesis. Previous studies have suggested that SNF5 suppresses cancer by signaling through the p16Ink4a and retinoblastoma tumor suppressors to negatively regulate cell cycle progression from G0/G1 into S phase. A recent paper in Genes and Development (Vries et al., 2005) reports that human SNF5 also signals via the p16INK4a-Rb-E2F pathway to regulate chromosomal stability, suggesting a new function for this chromatin remodeling protein in tumor suppression. | |
| dc.language.iso | en_US | |
| dc.relation | <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=15837618&dopt=Abstract">Link to Article in PubMed</a> | |
| dc.relation.url | http://dx.doi.org/10.1016/j.ccr.2005.04.001 | |
| dc.subject | Aneuploidy | |
| dc.subject | Animals | |
| dc.subject | Cell Cycle | |
| dc.subject | Cell Cycle Proteins | |
| dc.subject | Chromatin Assembly and Disassembly | |
| dc.subject | Chromosomal Instability | |
| dc.subject | Chromosomal Proteins, Non-Histone | |
| dc.subject | Cyclin D1 | |
| dc.subject | Cyclin-Dependent Kinase 4 | |
| dc.subject | Cyclin-Dependent Kinase Inhibitor p16 | |
| dc.subject | Cyclin-Dependent Kinases | |
| dc.subject | DNA-Binding Proteins | |
| dc.subject | E2F Transcription Factors | |
| dc.subject | Humans | |
| dc.subject | Models, Biological | |
| dc.subject | Phosphorylation | |
| dc.subject | Polyploidy | |
| dc.subject | Proto-Oncogene Proteins | |
| dc.subject | Retinoblastoma Protein | |
| dc.subject | Rhabdoid Tumor | |
| dc.subject | Transcription Factors | |
| dc.subject | Tumor Suppressor Proteins | |
| dc.subject | Cell Biology | |
| dc.title | Snf5 tumor suppressor couples chromatin remodeling, checkpoint control, and chromosomal stability | |
| dc.type | Journal Article | |
| dc.source.journaltitle | Cancer cell | |
| dc.source.volume | 7 | |
| dc.source.issue | 4 | |
| dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/jones/21 | |
| dc.identifier.contextkey | 1750955 | |
| html.description.abstract | <p>SNF5 is a core subunit of the SWI/SNF chromatin-remodeling complex. Mammalian SNF5 is essential for normal cell viability, and loss or mutation of the human SNF gene is the molecular basis for familial malignant rhabdoid tumorigenesis. Previous studies have suggested that SNF5 suppresses cancer by signaling through the p16Ink4a and retinoblastoma tumor suppressors to negatively regulate cell cycle progression from G0/G1 into S phase. A recent paper in Genes and Development (Vries et al., 2005) reports that human SNF5 also signals via the p16INK4a-Rb-E2F pathway to regulate chromosomal stability, suggesting a new function for this chromatin remodeling protein in tumor suppression.</p> | |
| dc.identifier.submissionpath | jones/21 | |
| dc.contributor.department | Department of Cell Biology | |
| dc.source.pages | 294-5 |
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