In vitro, in vivo and in silico evidence suggests that bacteria exploit intrinsic chromosomal fluctuations to achieve intracellular transport.

Cellular carbon accumulation systems are a fundamental prerequisite for biomineralization to stabilize pH and to supply inorganic carbon for CaCO₃ precipitation under changing environmental conditions.

A quantitative analysis of glucose-dependent transport regulation indicates that mitochondrial accumulation in regions of high nutrient availability can enhance metabolism in neuronal axons under physiologically relevant conditions.

Dynein bypasses obstacles on microtubules more efficiently than single kinesin, and kinesins overcome this limitation when transporting intracellular cargos in teams.

Excess membrane can trap outgoing extracellular matrix proteins in secreting cells, leading to pericellular deposits that cause tissue damage.

T antigen glycosylation, which marks metastatic cancer cells, is modulated on a small set of proteins by a conserved multipass transmembrane protein to allow tissue invasion by Drosophila macrophages.

Unlike other cytoskeletal motors that produce torque in a specific direction, cytoplasmic dynein generates torque in either direction, resulting in bidirectional helical motility along microtubules.

Biochemical analysis reveals molecular mechanisms underlying the activation of the mitochondrial Ca²⁺ uniporter by intracellular Ca²⁺ signals.

A simple model of active transport in neurons allows intracellular cargo to find sites of demand using only local signals, but predicts long delays in distributing cargo throughout a dendritic tree.

The pseudoenzyme CPT1C is able to sense changes in intracellular malonyl-CoA levels caused by nutrients or energy stress and regulate late endosomes/lysosomes anterograde transport, necessary for proper axon growth.