Saliva performs a number of extremely important biological functions that are instrumental in maintaining oralhealth. It has been estimated that more than 5 million people in the US suffers from salivary gland dysfunction(Sjogren's syndrome). Although no genes mutations have been identified that could explain the pathogenesisof Sjogren's syndrome (SS), recent evidence have suggested that T17-cell infiltration and induction ofapoptosis in salivary gland acinar cells could be the two major events that could lead to salivary glanddestruction.

Phenylalanine hydroxylase (PheH) catalyzes the hydroxylation of dietary phenylalanine to tyrosine. Lack of a functional PheH results in the metabolic disease phenylketonuria (PKU). PheH is one of three aromatic amino acid hydroxylases; the other two are tyrosine hydroxylase and tryptophan hydroxylase. Regulation of PheH is tightly controlled so that only excess phenylalanine is consumed. The enzyme is regulated by activation by phenylalanine, inhibition by tetrahydrobiopterin (BH4), and phosphorylation at Ser16.

Acute kidney injury (AKI) is a common event associated with high morbidity and mortality. Ischemia is a major cause of AKI. TRPM2, a member of the transient receptor potential- melastatin subfamily, is activated by oxidant stress, ADP-ribose, TNF and intracellular calcium, all of which are increased during kidney ischemia. We found that genetic or pharmacologic inhibition of TRPM2 dramatically reduces ischemic kidney injury. The mechanism involves, at least in part, a TRPM2-dependent increase in Rac1 activity resulting in increased NADPH oxidase activity and oxidant stress.