Dysfunction of lamin A triggers a DNA damage response and cellular senescence
- 3 February 2006
- journal article
- review article
- Published by Elsevier in DNA Repair
- Vol. 5 (2) , 286-289
- https://doi.org/10.1016/j.dnarep.2005.10.007
Abstract
No abstract availableKeywords
This publication has 23 references indexed in Scilit:
- Deficient DNA repair in the human progeroid disorder, Werner syndromeMutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 2005
- Genome instability in progeria: when repair gets oldNature Medicine, 2005
- The nuclear lamina comes of ageNature Reviews Molecular Cell Biology, 2005
- The Function of Nuclear Architecture: A Genetic ApproachAnnual Review of Genetics, 2004
- LMNA mutations in atypical Werner's syndromeThe Lancet, 2003
- A progeroid syndrome in mice is caused by defects in A-type laminsNature, 2003
- Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defectProceedings of the National Academy of Sciences, 2002
- Life at the edge: the nuclear envelope and human diseaseNature Reviews Molecular Cell Biology, 2002
- Remodelling the walls of the nucleusNature Reviews Molecular Cell Biology, 2002
- Defective prelamin A processing and muscular and adipocyte alterations in Zmpste24 metalloproteinase–deficient miceNature Genetics, 2002