Angela Woods

TL;DR: It is shown in mice that deletion of ribosomal S6 protein kinase 1 (S6K1), a component of the nutrient-responsive mTOR (mammalian target of rapamycin) signaling pathway, led to increased life span and resistance to age-related pathologies, such as bone, immune, and motor dysfunction and loss of insulin sensitivity.

TL;DR: It is shown that AMPKK phosphorylates at least two other sites on the alpha subunit and one site on the beta subunit, and evidence that phosphorylation of Thr(172) may be involved in the sensitivity of the AMPK complex to AMP is provided.

TL;DR: Three yeast kinases are identified that activate Snf1 kinase in vivo and it is shown that the closely related mammalian LKB1 kinases, which is associated with Peutz–Jeghers cancer-susceptibility syndrome, phosphorylates and activates AMPK in vitro.

TL;DR: The observed differences in the regulation of alpha1 and alpha2 complexes by AMP might result in differential responses to ATP depletion in distinct cellular and subcellular locations.

TL;DR: The results suggest that AMPK is involved in the inhibition of glucose-activated gene expression but not in the induction pathway, and demonstrates that the two mutants generated will provide valuable tools for studying the wider physiological role of AMPK.