Differential expression patterns of sodium potassium ATPase alpha and beta subunit isoforms in mouse brain during postnatal development.

The sodium potassium ATPase (Na/K ATPase) is essential for the maintenance of a low intracellular Na and a high intracellular K concentration. Loss of function of the Na/K ATPase due to mutations in Na/K ATPase genes, anoxic conditions, depletion of ATP or inhibition of the Na/K ATPase function using cardiac glycosides such as digitalis, causes a depolarization of the resting membrane potential. While in non-excitable cells, the uptake of glucose and amino acids is decreased if the function of the Na/K ATPase is compromised, in excitable cells the symptoms range from local hyper-excitability to inactivating depolarization.

Ras and rheb signaling in survival and cell death.

One of the most obvious hallmarks of cancer is uncontrolled proliferation of cells partly due to independence of growth factor supply. A major component of mitogenic signaling is Ras, a small GTPase. It was the first identified human protooncogene and is known since more than three decades to promote cellular proliferation and growth.

Hyperoxia changes the balance of the thioredoxin/peroxiredoxin system in the neonatal rat brain.

Reactive oxygen species (ROS) and intrinsic antioxidant defense systems play an important role in both physiological cell signaling processes and many pathological states, including neurodegenerative disorders and oxygen-toxicity. Here we report that short exposures to non-physiologic oxygen levels change the balance of the ROS-dependent thioredoxin/peroxiredoxin system in the developing rat brain. The aim of this study was to evaluate the expression of peroxiredoxins, thioredoxin 1, sulfiredoxin 1, and DJ-1 on gene and protein level under hyperoxic conditions.