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Cited by 1,125

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Lamin A-Dependent Nuclear Defects in Human Aging

Scaffidi, Paola, Misteli, Tom·2006·Science
DOI 10.1126/science.1127168
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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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Crossref · 10.1126/science.1127168

Cites

3 of 3 references verified0 citation errors · 0 not checkable

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  • Alterations of the nuclear lamina and production of an aberrant prelamin A isoform called progerin have been detected during normal human aging.

    “Alterations of the nuclear lamina and production of an aberrant prelamin A isoform called progerin have also been detected during normal human aging (Ragnauth et al., 2010; Scaffidi and Misteli, 2006).”

    From The Hallmarks of Aging (2013) · cites this paper as Scaffidi and Misteli, 2006

  • H3K9me3 is a histone modification associated with heterochromatin that has been previously shown to be reduced globally with age in a number of organisms, including in human fibroblasts.

    “H3K9me3 is a histone modification associated with heterochromatin that has been previously shown to be reduced globally with age in a number of organisms (Ni et al., 2012), including in human fibroblasts (O’Sullivan et al., 2010; Scaffidi and Misteli, 2006).”

    From Multi-omic rejuvenation of human cells by maturation phase transient reprogramming (2022) · cites this paper as Scaffidi and Misteli, 2006

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Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 11

  1. 10.1038/nrm950 · DOI
  2. 10.1126/science.1084125 · DOI · Paper page
  3. 10.1038/nature01629 · DOI · Paper page
  4. 10.1073/pnas.0402943101 · DOI · Paper page
  5. 10.1038/nm1204 · DOI · Paper page
  6. W. Andrew, Adv. Gerontol. Res.18, 87 (1964).
  7. 10.1073/pnas.0506955102 · DOI
  8. 10.1038/ncb1095 · DOI · Paper page
  9. 10.1194/jlr.R500011-JLR200 · DOI
  10. 10.1073/pnas.0504641102 · DOI
  11. 10.1074/jbc.271.16.9249 · DOI

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Metadata

Authors
Scaffidi, P., & Misteli, T.
Affiliations
National Cancer Institute (NCI), NIH, Bethesda, MD 20892, USA.
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
2006-05-19
Volume
312
Issue
5776
Pages
1059-1063
ISSN
  • 0036-8075
  • 1095-9203
DOI
10.1126/science.1127168
Cited by
1,125
References
3
Language
en

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