| pubmed-article:14755273 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:14755273 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:14755273 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:14755273 | lifeskim:mentions | umls-concept:C0001811 | lld:lifeskim |
| pubmed-article:14755273 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:14755273 | lifeskim:mentions | umls-concept:C0012854 | lld:lifeskim |
| pubmed-article:14755273 | lifeskim:mentions | umls-concept:C0221198 | lld:lifeskim |
| pubmed-article:14755273 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:14755273 | pubmed:dateCreated | 2004-2-2 | lld:pubmed |
| pubmed-article:14755273 | pubmed:abstractText | Humans and animals undergo ageing, and although their primary cells undergo cellular senescence in culture, the relationship between these two processes is unclear. Here we show that gamma-H2AX foci (gamma-foci), which reveal DNA double-strand breaks (DSBs), accumulate in senescing human cell cultures and in ageing mice. They colocalize with DSB repair factors, but not significantly with telomeres. These cryptogenic gamma-foci remain after repair of radiation-induced gamma-foci, suggesting that they may represent DNA lesions with unrepairable DSBs. Thus, we conclude that accumulation of unrepairable DSBs may have a causal role in mammalian ageing. | lld:pubmed |
| pubmed-article:14755273 | pubmed:language | eng | lld:pubmed |
| pubmed-article:14755273 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14755273 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:14755273 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14755273 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14755273 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:14755273 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:14755273 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:14755273 | pubmed:issn | 1465-7392 | lld:pubmed |
| pubmed-article:14755273 | pubmed:author | pubmed-author:BarrettJ... | lld:pubmed |
| pubmed-article:14755273 | pubmed:author | pubmed-author:BonnerWilliam... | lld:pubmed |
| pubmed-article:14755273 | pubmed:author | pubmed-author:PopescuNichol... | lld:pubmed |
| pubmed-article:14755273 | pubmed:author | pubmed-author:HorikawaIzumi... | lld:pubmed |
| pubmed-article:14755273 | pubmed:author | pubmed-author:SedelnikovaOl... | lld:pubmed |
| pubmed-article:14755273 | pubmed:author | pubmed-author:ZimonjicDraze... | lld:pubmed |
| pubmed-article:14755273 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:14755273 | pubmed:volume | 6 | lld:pubmed |
| pubmed-article:14755273 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:14755273 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:14755273 | pubmed:pagination | 168-70 | lld:pubmed |
| pubmed-article:14755273 | pubmed:dateRevised | 2005-11-21 | lld:pubmed |
| pubmed-article:14755273 | pubmed:meshHeading | pubmed-meshheading:14755273... | lld:pubmed |
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| pubmed-article:14755273 | pubmed:meshHeading | pubmed-meshheading:14755273... | lld:pubmed |
| pubmed-article:14755273 | pubmed:meshHeading | pubmed-meshheading:14755273... | lld:pubmed |
| pubmed-article:14755273 | pubmed:meshHeading | pubmed-meshheading:14755273... | lld:pubmed |
| pubmed-article:14755273 | pubmed:meshHeading | pubmed-meshheading:14755273... | lld:pubmed |
| pubmed-article:14755273 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:14755273 | pubmed:articleTitle | Senescing human cells and ageing mice accumulate DNA lesions with unrepairable double-strand breaks. | lld:pubmed |
| pubmed-article:14755273 | pubmed:affiliation | Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA. | lld:pubmed |
| pubmed-article:14755273 | pubmed:publicationType | Journal Article | lld:pubmed |
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