| pubmed-article:16537910 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C1704461 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C1167087 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C0292369 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C0012860 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C1333030 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C0312418 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C0812273 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C0205217 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C1335840 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C0036667 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C1711351 | lld:lifeskim |
| pubmed-article:16537910 | lifeskim:mentions | umls-concept:C1548534 | lld:lifeskim |
| pubmed-article:16537910 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:16537910 | pubmed:dateCreated | 2006-3-15 | lld:pubmed |
| pubmed-article:16537910 | pubmed:abstractText | The gene encoding the SNF5/Ini1 core subunit of the SWI/SNF chromatin remodeling complex is a tumor suppressor in humans and mice, with an essential role in early embryonic development. To investigate further the function of this gene, we have generated a Cre/lox-conditional mouse line. We demonstrate that Snf5 deletion in primary fibroblasts impairs cell proliferation and survival without the expected derepression of most retinoblastoma protein-controlled, E2F-responsive genes. Furthermore, Snf5-deficient cells are hypersensitive to genotoxic stress, display increased aberrant mitotic features, and accumulate phosphorylated p53, leading to elevated expression of a specific subset of p53 target genes, suggesting a role for Snf5 in the DNA damage response. p53 inactivation does not rescue the proliferation defect caused by Snf5 deficiency but reduces apoptosis and strongly accelerates tumor formation in Snf5-heterozygous mice. | lld:pubmed |
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