The ATM kinase has an unanticipated role in tumor progression through the regulation of cell migration by oxidative stress.

Mutations within the ATPase domain of RIG-I in patients with Singleton-Merten Syndrome prevent ATP-hydrolysis dependent dissociation of RIG-I from double-stranded RNA and lead to unintentional constitutive signaling through increased binding of endogenous RNA.

Visualization of BRM remodelers engaging their endogenous genomic targets revealed highly transient and dynamic interactions with chromatin, which are fueled by ATP-hydrolysis.

BRG1 loss drives initiation and progression in human cancers through changes in specific differentiation programs in an AP-1-dependent manner.

MgADP binding to the high-affinity 'consensus' ATPase active site of SUR1 and remodeling of the L0-loop (lasso region) overrides tonic ATP inhibition of KATP channels.

The accumulation of its product, cytidine triphosphate, encourages the enzyme CTP synthetase (CtpS) to form large-scale polymers and inhibits the enzyme's activity.

A molecular model that provides a framework for interpreting the wealth of functional information obtained on the E. coli F-ATP synthase has been generated using cryo-electron microscopy.

Deletion of the ATM cofactor ATMIN reduces PDGFRA expression and strongly suppresses tumorigenesis in a TP53-deficient mouse model of glioblastoma.

The ATM-SIRT6 axis integrates the DNA repair machinery to longevity-promoting pathways.

Structural analysis of the ATP synthase – in combination with evolutionary covariance analysis – reveals the fold of the a subunit and shows that the enzyme can adopt several different conformations, which support the Brownian ratchet model for generating rotation.