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- David Kipling
- Department of Pathology, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
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- Terence Davis
- Department of Pathology, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
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- Elizabeth L. Ostler
- Department of Pathology, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
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- Richard G. A. Faragher
- Department of Pathology, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
書誌事項
- 公開日
- 2004-09-03
- DOI
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- 10.1126/science.1102587
- 公開者
- American Association for the Advancement of Science (AAAS)
この論文をさがす
説明
<jats:p>Human genetic diseases that resemble accelerated aging provide useful models for gerontologists. They combine known single-gene mutations with deficits in selected tissues that are reminiscent of changes seen during normal aging. Here, we describe recent progress toward linking molecular and cellular changes with the phenotype seen in two of these disorders. One in particular, Werner syndrome, provides evidence to support the hypothesis that the senescence of somatic cells may be a causal agent of normal aging.</jats:p>
収録刊行物
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- Science
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Science 305 (5689), 1426-1431, 2004-09-03
American Association for the Advancement of Science (AAAS)
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詳細情報 詳細情報について
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- CRID
- 1362544418435286016
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- NII論文ID
- 30020391745
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- ISSN
- 10959203
- 00368075
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- データソース種別
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- Crossref
- CiNii Articles