The H+ influx coupled to nutrient uptake and the plasma membrane H+-ATPase are central actors of the activation of target of rapamycin complex 1 (TORC1) in budding yeast Saccharomyces cerevisiae..

An unbiased genome-wide human forward genetic screen identifies the vacuolar ATPase complex and assembly factors as regulators of HIF stability through their actions on intracellular iron metabolism.

Genetic labeling of cells that survive executioner caspase activity in Drosophila reveals distinct patterns in different tissues.

The human Origin Replication Complex is shaped as a shallow corkscrew in a classic AAA+ organization reminiscent of clamp loader complexes with highly controlled ATPase activity as exemplified by Meier-Gorlin syndrome mutations.

DNA synthesis by DNA polymerase V is regulated by an intrinsic DNA-dependent ATPase activity which has not been observed for any other polymerase.

Cryo-EM structures of rotary V-ATPase reveal the ON-OFF switching mechanism of H⁺ translocation in the V_o membrane domain.

Biochemical and structural analyses of a universal mRNP remodeling pathway suggest an ATPase-powered targeted deposition of export factors onto mRNP.

A broadly used gene expression regulatory mechanism inactivates targets by CED-3-caspase-mediated proteolysis and works in parallel to miRNAs for diverse non-apoptotic developmental functions.

Parallel measurements of pH gradient and membrane potential at the single vesicle level have revealed that the synaptic vesicle acidification is initiated by removal of its clathrin coat, which blocks vesicular ATPase activity.

Myc expression is shown to cause sublethal activation of Caspase-3 and downstream endonuclease G, which causes DNA double strand breaks and oncogenic transformation in human cells.