Nucleoplasmic LAP2α–lamin A complexes are required to maintain a proliferative state in human fibroblasts

por Pekovic, Vanja, Harborth, Jens, Broers, Jos L.V., Ramaekers, Frans C.S., van Engelen, Baziel, Lammens, Martin, von Zglinicki, Thomas, Foisner, Roland, Hutchison, Chris, Markiewicz, Ewa
Publicado 2007

Soft substrates normalize nuclear morphology and prevent nuclear rupture in fibroblasts from a laminopathy patient with compound heterozygous LMNA mutations

por Tamiello, Chiara, Kamps, Miriam A.F., van den Wijngaard, Arthur, Verstraeten, Valerie L. R. M., Baaijens, Frank P.T., Broers, Jos L.V., Bouten, Carlijn C.V.
Publicado 2013

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

por Sieprath, Tom, Corne, Tobias DJ, Nooteboom, Marco, Grootaert, Charlotte, Rajkovic, Andreja, Buysschaert, Benjamin, Robijns, Joke, Broers, Jos LV, Ramaekers, Frans CS, Koopman, Werner JH, Willems, Peter HGM, De Vos, Winnok H
Publicado 2015

The R439C mutation in LMNA causes lamin oligomerization and susceptibility to oxidative stress

por Verstraeten, Valerie LRM, Caputo, Sandrine, Van Steensel, Maurice AM, Duband-Goulet, Isabelle, Zinn-Justin, Sophie, Kamps, Miriam, Kuijpers, Helma JH, Östlund, Cecilia, Worman, Howard J, Briedé, Jacob J, Le Dour, Caroline, Marcelis, Carlo LM, Van Geel, Michel, Steijlen, Peter M, Van Den Wijngaard, Arthur, Ramaekers, Frans CS, Broers, Jos LV
Publicado 2009