AMP-activated protein kinase directly coordinates glutamatergic signalling during starvation in C. elegans.

An effector of AMPK is essential for the kinase and its pharmacological activators, including Metformin, to strengthen cell-cell junctions and preserve epithelial cell polarity and barrier functions in the face of energetic stress, as well as to suppress oncogenesis.

The conserved AMP-activated protein kinase inhibits mitochondrial import of misfolded proteins and helps preserve mitochondrial and cellular fitness under proteotoxic stress.

A genetic knock-in mouse model reveals that the endocrine state governs the effect of the common fatty acid amide hydrolase C385A variant on body weight through a hypothalamic-mediated mechanism.

Autophagy and Lkb1 work synergistically to maintain adult mouse homeostasis and survival.

Modulating the nutrient sensor TORC1 only in neurons in C. elegans is sufficient to regulate systemic longevity via inter-tissue signals that remodel mitochondria networks in non neuronal cells.

The first demonstration that cellular ATP homeostasis suppresses high volatility of cellular ATP levels to ensure proteostasis that prevents accumulation of cytotoxic protein aggregation.

Yeast Nuak1 is an AMPK and CK2 dependent H3 T11 kinase.

Single-cell data on cell signaling responses to nutrient variation enable quantitative models of cellular control over protein synthesis, formalizing the concept of mTOR as a homeostatic controller of cellular metabolism.

A non-canonical p53 function in adipocyte plays a critical role in energy homeostasis and is involved in obesity-associated metabolic dysfunctions.