Sustained accumulation of prelamin A and depletion of lamin A/C both cause oxidative stress and mitochondrial dysfunction but induce different cell fates

Tom Sieprath, Tobias D. J. Corne, Marco Nooteboom, Charlotte Grootaert, Andreja Rajkovic, Benjamin Buysschaert, Joke Robijns, Jos L. V. Broers, Frans C. S. Ramaekers, Werner J. H. Koopman, Peter H. G. M. Willems, Winnok H. De Vos

Research output: Contribution to journalArticleAcademicpeer-review

7 Citations (Scopus)
Original languageEnglish
Pages (from-to)236-246
JournalNucleus-austin
Volume6
Issue number3
DOIs
Publication statusPublished - 2015

Keywords

  • apoptosis
  • high-content microscopy
  • lamin A
  • C
  • laminopathies
  • mitochondria
  • mitochondrial dysfunction
  • oxidative stress
  • prelamin A
  • senescence
  • ZMPSTE24

Cite this

Sieprath, T., Corne, T. D. J., Nooteboom, M., Grootaert, C., Rajkovic, A., Buysschaert, B., Robijns, J., Broers, J. L. V., Ramaekers, F. C. S., Koopman, W. J. H., Willems, P. H. G. M., & De Vos, W. H. (2015). Sustained accumulation of prelamin A and depletion of lamin A/C both cause oxidative stress and mitochondrial dysfunction but induce different cell fates. Nucleus-austin, 6(3), 236-246. https://doi.org/10.1080/19491034.2015.1050568