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| pubmed-article:10959836 | pubmed:issue | 15 | lld:pubmed |
| pubmed-article:10959836 | pubmed:dateCreated | 2000-11-15 | lld:pubmed |
| pubmed-article:10959836 | pubmed:abstractText | The response of eukaryotic cells to double-strand breaks in genomic DNA includes the sequestration of many factors into nuclear foci. Recently it has been reported that a member of the histone H2A family, H2AX, becomes extensively phosphorylated within 1-3 minutes of DNA damage and forms foci at break sites. | lld:pubmed |
| pubmed-article:10959836 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10959836 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10959836 | pubmed:issn | 0960-9822 | lld:pubmed |
| pubmed-article:10959836 | pubmed:author | pubmed-author:BonnerW MWM | lld:pubmed |
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| pubmed-article:10959836 | pubmed:author | pubmed-author:RogakouE PEP | lld:pubmed |
| pubmed-article:10959836 | pubmed:author | pubmed-author:YamazakiVV | lld:pubmed |
| pubmed-article:10959836 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10959836 | pubmed:volume | 10 | lld:pubmed |
| pubmed-article:10959836 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10959836 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10959836 | pubmed:pagination | 886-95 | lld:pubmed |
| pubmed-article:10959836 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:10959836 | pubmed:articleTitle | A critical role for histone H2AX in recruitment of repair factors to nuclear foci after DNA damage. | lld:pubmed |
| pubmed-article:10959836 | pubmed:affiliation | Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-0540, USA. | lld:pubmed |
| pubmed-article:10959836 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10959836 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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