A newly discovered cytoplasmic intermediate filament in water bears may help these animals to resist extreme environmental conditions.

Expression of the lamina-associated polypeptide α (LAP2α) prevents premature cellular ageing caused by expression of progerin in Hutchinson-Gilford progeria syndrome.

The lamin A/C binding protein LAP2α inhibits formation of higher order lamin structures in the nuclear interior in a lamin A/C-phosphorylation-independent manner, thereby regulating chromatin mobility.

Lamin B receptor may provide a long-sought model system enabling unprecedented studies of protein quality control in the nuclear envelope of mammalian cells.

Age-stratified comparisons of gene expression in progeria patient fibroblasts reveals disruption of mesenchymal lineage pathways and points to a deficit in chondrogenic commitment in early development and a depletion of the mesenchymal lineage stem cell pool.

The polo-like kinase (Plk1) phophorylates the C. elegans lamin LMN-1 to promote timely lamina disassembly, which is essential for the merging of the parental chromosomes at the beginning of life.

Hey together with LaminC continuously supervise nuclear organisation and differentiated enterocyte identity, a regulation that is lost upon ageing, resulting in loss of gut homeostasis.

A comprehensive molecular description of the cellular transition into replicative senescence provides evidence of metabolic, epigenetic, and regulatory rewiring that links senescence with wound healing and fibrosis.

Chromatin modifiers shape nuclear morphology.

Nuclear reorganization and stiffening accompanies mesenchymal stem cell differentiation, resulting in increased sensitivity to mechanical perturbation.