Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation-Reference-Cited by-同舟云学术

Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation

Published:2005-08-03 Issue:7058 Volume:437 Page:564-568
ISSN:0028-0836
Container-title:Nature
language:en
Short-container-title:Nature

Author:

Varela Ignacio,Cadiñanos Juan,Pendás Alberto M.,Gutiérrez-Fernández Ana,Folgueras Alicia R.,Sánchez Luis M.,Zhou Zhongjun,Rodríguez Francisco J.,Stewart Colin L.,Vega José A,Tryggvason Karl,Freije José M. P.,López-Otín Carlos

Publisher

Springer Science and Business Media LLC

Subject

Multidisciplinary

Link

http://www.nature.com/articles/nature04019.pdf

Reference30 articles.

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2. Bergo, M. O. et al. Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect. Proc. Natl Acad. Sci. USA 99, 13049–13054 (2002)

3. Corrigan, D. P. et al. Prelamin A endoproteolytic processing in vitro by recombinant Zmpste24. Biochem. J. 387, 129–138 (2005)

4. Sullivan, T. et al. Loss of A-type lamin expression compromises nuclear envelope integrity leading to muscular dystrophy. J. Cell Biol. 147, 913–920 (1999)

5. Mounkes, L. C., Kozlov, S., Hernandez, L., Sullivan, T. & Stewart, C. L. A progeroid syndrome in mice is caused by defects in A-type lamins. Nature 423, 298–301 (2003)

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