Enterovirus D68, a pathogen associated with a rare child paralysis disease, depends on the cellular protein SIRT-1 for release of virus, indicating that SIRT-1 may be an important therapeutic target.

SIRT2 has detrimental effects in the heart and plays a role in cardiac response to injury and the progression of cardiac hypertrophy, and targeting SIRT2 may provide a novel avenue for the treatment of cardiac hypertrophy and ischemic disease.

SIRT1 and SIRT3-mediated immunometabolic shift governs intracellular Salmonella proliferation both in vitro and in vivo and dissemination in mice, thereby influencing the infection outcomes.

A novel phenotypic screening platform based on immunofluorescent imaging of histone modifications enables accurate identification of cell fates and environmental perturbations.

Sirt3 functions as decrotonylase to regulate histone crotonylation dynamics.

Interactions were visualized between the nuclear egress complex from herpes simplex virus and a capsid protein that could promote nucleocytoplasmic translocation of the capsid in infected cells.

Mass spectroscopy, molecular modeling and/or molecular dynamics simulations reveal how acetylation regulates the activity of GSK3 isoforms independent of inhibitory phosphorylation.

A series of experiments at the molecular level reveal the underlying mechanism of how a gene activates liver glucose production to regulate the blood glucose metabolism in mice.

An atomic model of the bacterial chemosensory array obtained through the synthesis of cryo-electron tomography and large-scale molecular-dynamics simulations reveals a new kinase conformation during signaling events.

A correlation between the periplasmic embellishment of the flagellar motor and its stator system type is described, motors with dual H+-dependent stator systems have one periplasmic ring formed by MotY.