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      Lamin A-dependent nuclear defects in human aging.

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          Abstract

          Mutations in the nuclear structural protein lamin A cause the premature aging syndrome Hutchinson-Gilford progeria (HGPS). Whether lamin A plays any role in normal aging is unknown. We show that the same molecular mechanism responsible for HGPS is active in healthy cells. Cell nuclei from old individuals acquire defects similar to those of HGPS patient cells, including changes in histone modifications and increased DNA damage. Age-related nuclear defects are caused by sporadic use, in healthy individuals, of the same cryptic splice site in lamin A whose constitutive activation causes HGPS. Inhibition of this splice site reverses the nuclear defects associated with aging. These observations implicate lamin A in physiological aging.

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          Author and article information

          Journal
          Science
          Science (New York, N.Y.)
          American Association for the Advancement of Science (AAAS)
          1095-9203
          0036-8075
          May 19 2006
          : 312
          : 5776
          Affiliations
          [1 ] National Cancer Institute (NCI), NIH, Bethesda, MD 20892, USA.
          Article
          1127168 NIHMS18672
          10.1126/science.1127168
          1855250
          16645051
          b1b6141a-025b-417f-8d90-edf94758d3aa
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