@article{11069,
  abstract     = {Repeated rounds of nuclear envelope (NE) rupture and repair have been observed in laminopathy and cancer cells and result in intermittent loss of nucleus compartmentalization. Currently, the causes of NE rupture are unclear. Here, we show that NE rupture in cancer cells relies on the assembly of contractile actin bundles that interact with the nucleus via the linker of nucleoskeleton and cytoskeleton (LINC) complex. We found that the loss of actin bundles or the LINC complex did not rescue nuclear lamina defects, a previously identified determinant of nuclear membrane stability, but did decrease the number and size of chromatin hernias. Finally, NE rupture inhibition could be rescued in cells treated with actin-depolymerizing drugs by mechanically constraining nucleus height. These data suggest a model of NE rupture where weak membrane areas, caused by defects in lamina organization, rupture because of an increase in intranuclear pressure from actin-based nucleus confinement.},
  author       = {Hatch, Emily M. and HETZER, Martin W},
  issn         = {0021-9525},
  journal      = {Journal of Cell Biology},
  keywords     = {Cell Biology},
  number       = {1},
  pages        = {27--36},
  publisher    = {Rockefeller University Press},
  title        = {{Nuclear envelope rupture is induced by actin-based nucleus confinement}},
  doi          = {10.1083/jcb.201603053},
  volume       = {215},
  year         = {2016},
}

@article{11081,
  abstract     = {In eukaryotic cells the nuclear genome is enclosed by the nuclear envelope (NE). In metazoans, the NE breaks down in mitosis and it has been assumed that the physical barrier separating nucleoplasm and cytoplasm remains intact during the rest of the cell cycle and cell differentiation. However, recent studies suggest that nonmitotic NE remodeling plays a critical role in development, virus infection, laminopathies, and cancer. Although the mechanisms underlying these NE restructuring events are currently being defined, one common theme is activation of protein kinase C family members in the interphase nucleus to disrupt the nuclear lamina, demonstrating the importance of the lamina in maintaining nuclear integrity.},
  author       = {Hatch, Emily and HETZER, Martin W},
  issn         = {1540-8140},
  journal      = {Journal of Cell Biology},
  keywords     = {Cell Biology},
  number       = {2},
  pages        = {133--141},
  publisher    = {Rockefeller University Press},
  title        = {{Breaching the nuclear envelope in development and disease}},
  doi          = {10.1083/jcb.201402003},
  volume       = {205},
  year         = {2014},
}