Philipp Isermann

TL;DR: Investigation of mammalian tumor cell migration in confining microenvironments in vitro and in vivo indicates that cell migration incurs substantial physical stress on the NE and its content and requires efficient NE and DNA damage repair for cell survival.

TL;DR: An overview of how LINC complex proteins and lamins facilitate nucleo-cytoskeletal coupling is provided, recent findings regarding the role of the nucleus in cellular mechanotransduction and cell motility in 3D environments are highlighted, and mutations and/or changes in the expression of these nuclear envelope proteins are discussed.

TL;DR: The results indicate that although defective nuclear stability may play a role in the development of muscle diseases, other factors, such as impaired nucleo-cytoskeletal coupling, likely contribute to the muscle phenotype.

TL;DR: Use of three mouse models of muscle laminopathies and muscle biopsies from individuals with LMNA -related muscular dystrophy found that Lmna mutations reduced nuclear stability and caused transient rupture of the NE in skeletal muscle cells, resulting in DNA damage, DNA damage response activation and reduced cell viability.

TL;DR: The design of a polydimethylsiloxane (PDMS) microfluidic device composed of channels with precisely-defined constrictions mimicking physiological environments that enable high resolution imaging of live and fixed cells is described, revealing distinct phases of nuclear translocation through the constriction, buckling of the nuclear lamina, and severe intranuclear strain.