Mitochondrial flashes counteract the imbalance of ATP supply-and-demand and constitute an auto-regulator of ATP homeostasis in the heart.

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

Mitochondrial Cx43 hemichannels regulate ATP generation by mediating K+, H+, and ATP transfer across the mitochondrial inner membrane and the interaction with mitochondrial ATP synthase, contributing to maintenance of mitochondrial redox and cell protection under oxidative stress.

Biochemical and in vivo physiology imaging reveal that plant pathogens actively imbalance the apoplastic eAdo/eATP levels as a virulence mechanism.

ATP imaging of spiking optic nerve axons in real time reveals correlation between ATP levels and electrical activity as well as contribution of lactate metabolism to axonal ATP homeostasis.

Genetic and biochemical analysis of two enzymes reveals that inositol pyrophosphate signaling molecules allow plants to sense and regulate cellular phosphate levels, and to take up more phosphate when needed.

Mammalian cellular iron homeostasis and the maturation of the cytosolic iron sulfur cluster proteins are dependent on the mitochondrial protein import machinery.

Two distinct processes drive coordinated synthesis of purine and pyridine (NAD⁺) nucleotides in response to AICAR derivatives and ATP.

Animal models reveal that mitochondrial complex I is dispensable for homeostatic functions of the mouse liver.

ATP enters the endoplasmic reticulum (ER) lumen through an SLC35B1/AXER-dependentCaATiER mechanism, and ATP usage in the ER renders 'anti-Warburg' effect by increasing ATP regeneration from OxPhos while decreasing glycolysis.