Genomic instability in laminopathy-based premature aging

@article{Liu2005GenomicII,
  title={Genomic instability in laminopathy-based premature aging},
  author={Baohua Liu and Jianming Wang and K. Chan and W. Tjia and W. Deng and Xinyuan Guan and J. Huang and K. Li and Pui Yin Chau and David J. Chen and D. Pei and A. Pend{\'a}s and J. Cadi{\~n}anos and C. L{\'o}pez-Ot{\'i}n and H. Tse and C. Hutchison and Junjie Chen and Yihai Cao and K. Cheah and K. Tryggvason and Zhongjun Zhou},
  journal={Nature Medicine},
  year={2005},
  volume={11},
  pages={780-785}
}
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… Expand
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  • O. Dreesen
  • Biology, Medicine
  • Biochemical Society transactions
  • 2020
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TLDR
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