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Specific molecular links that orchestrate growth signals and metabolic reprogramming to achieve tumorigenesis are identified as potential metabolic vulnerabilities in cancer treatment.

Live-cell imaging shows that the contractile acto-myosin network on the nuclear envelope remnant positions chromosomes in early mitosis to ensure efficient and correct interactions between chromosomes and the mitotic spindle.

The dynamic phosphorylation of autophagy component WIPI2B is critical to maintain autophagosome biogenesis in neurons, and ectopic expression of WIPI2B can restore rates of autophagosome biogenesis in aged neurons.

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.

The autophagy protein ATG2A tethers membranes and transfers lipids between them, suggesting that autophagosome membranes grow upon the acquisition of lipids from the ER through the ATG2A bridge.

A Tubby protein regulates ciliary membrane morphology and phosphoinositide composition in a context-dependent manner.

Compositional changes alter actin binding by phase separated T cell signaling clusters, enabling cluster movement by distinct actin networks.

Autophagy is critical for the turnover of inflammatory signaling complexes containing RHIM-domain proteins.

Airway cells are required for the maintenance of the adult mouse lung and for carcinogen-induced lung adenocarcinoma development, and are thus marked therapeutic targets.

Absolute quantification of cohesin, CTCF, NIPBL, WAPL and sororin in HeLa cells implies that some genomic cohesin and CTCF enrichment sites are unoccupied at any one time.