| pubmed-article:15980864 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15980864 | lifeskim:mentions | umls-concept:C0231341 | lld:lifeskim |
| pubmed-article:15980864 | lifeskim:mentions | umls-concept:C0919532 | lld:lifeskim |
| pubmed-article:15980864 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:15980864 | pubmed:dateCreated | 2005-7-14 | lld:pubmed |
| pubmed-article:15980864 | pubmed:abstractText | Premature aging syndromes often result from mutations in nuclear proteins involved in the maintenance of genomic integrity. Lamin A is a major component of the nuclear lamina and nuclear skeleton. Truncation in lamin A causes Hutchinson-Gilford progerial syndrome (HGPS), a severe form of early-onset premature aging. Lack of functional Zmpste24, a metalloproteinase responsible for the maturation of prelamin A, also results in progeroid phenotypes in mice and humans. We found that Zmpste24-deficient mouse embryonic fibroblasts (MEFs) show increased DNA damage and chromosome aberrations and are more sensitive to DNA-damaging agents. Bone marrow cells isolated from Zmpste24-/- mice show increased aneuploidy and the mice are more sensitive to DNA-damaging agents. Recruitment of p53 binding protein 1 (53BP1) and Rad51 to sites of DNA lesion is impaired in Zmpste24-/- MEFs and in HGPS fibroblasts, resulting in delayed checkpoint response and defective DNA repair. Wild-type MEFs ectopically expressing unprocessible prelamin A show similar defects in checkpoint response and DNA repair. Our results indicate that unprocessed prelamin A and truncated lamin A act dominant negatively to perturb DNA damage response and repair, resulting in genomic instability which might contribute to laminopathy-based premature aging. | lld:pubmed |
| pubmed-article:15980864 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15980864 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15980864 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15980864 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15980864 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:15980864 | pubmed:issn | 1078-8956 | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:ChenJunjieJ | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:PeiDuanqingD | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:TseHung FatHF | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:CaoYihaiY | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:TryggvasonKar... | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:López-OtínCar... | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:ChenDavid JDJ | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:ZhouZhongjunZ | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:CadiñanosJuan... | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:WangJianmingJ | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:DengWenW | lld:pubmed |
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| pubmed-article:15980864 | pubmed:author | pubmed-author:LiuBaohuaB | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:GuanXinyuanX | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:TjiaWai MuiWM | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:ChanKui... | lld:pubmed |
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| pubmed-article:15980864 | pubmed:author | pubmed-author:LiKai ManKM | lld:pubmed |
| pubmed-article:15980864 | pubmed:author | pubmed-author:ChauPui YinPY | lld:pubmed |
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| pubmed-article:15980864 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15980864 | pubmed:volume | 11 | lld:pubmed |
| pubmed-article:15980864 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15980864 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15980864 | pubmed:pagination | 780-5 | lld:pubmed |
| pubmed-article:15980864 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:15980864 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15980864 | pubmed:articleTitle | Genomic instability in laminopathy-based premature aging. | lld:pubmed |
| pubmed-article:15980864 | pubmed:affiliation | Department of Biochemistry, University of Hong Kong, 21 Sassoon Road, Hong Kong. | lld:pubmed |
| pubmed-article:15980864 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15980864 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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