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Rings of actin polymerisation that form around PIP3/Ras patches in the cell membrane drive the formation of macropinocytic cups.

Akt mediated S14 phosphorylation of Id2 augments its protein stability and growth cone localization, promoting growth cone formation and axon growth in the developing neuron and contributing to axon regeneration in the damaged hippocampus slice.

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

Profiling of fibroblasts across mammals captures differences in longevity at the level of global gene expression and metabolite levels and reveals pathways that define these differences.

A toxin is used to introduce an otherwise cell-impermeant fluorophore-antibody (or some thing which is equally specific) to bind to an intracellular protein which allows for super resolution imaging and single particle tracking inside the living cell.

Phosphorylation of a core trafficking component, the COPII coat subunit Sec24, regulates cross-talk between the secretory and autophagy machinery during starvation.

Genetic and biochemical approaches identify a new component of the cellular signaling machinery driving migration of limb muscle precursor cells during mouse embryogenesis and reveal the underlying molecular mechanism.

Calcium influx during acute cell stimulation triggers a global actin reset in mammalian cells, which is linked to plasma membrane repair and transcription and has implications for our understanding of cell migration, cancer, inflammation and cell stress response.

Lamellar and tubular cristae in mitochondria form by two different molecular pathways that form both involve F₁F_O-ATP synthase dimers and the MICOS complex, but formation of lamellar cristae also relies on Mgm1/Opa1.

The polyQ tract of pathogenic Huntingtin causes aggregation when expanded in Huntington’s disease, but its two flanking domains control its conformational landscape, proteostasis and neurotoxicity.