Browsing by Subject "Modulation"
Now showing 1 - 2 of 2
- Results Per Page
- Sort Options
Item Modulation of GABAA Receptor Function by Tyrosine Phosphorylation(1998-05-01) Fang, Mingjun; Glenn Dillon; Thomas Yorio; Eugene E. QuistMingjun, Fang. Modulation of GABAA Receptor Function by Tyrosine Phosphorylation. Master of Science (Biomedical Sciences), May, 1998, 32 pp., 6 illustrations, bibliography, 42 titles. The goal of this study was to determine the modulation of GABAA receptor function by tyrosine kinase phosphorylation, and to detect which subunit is phosphorylated to alter the GABA-induced chloride currents. From previous studies, we suggested that protein tyrosine phosphorylation may maintain GABAA receptor function. Here we tested the hypothesis that tyrosine phosphorylation modulates other GABAA receptor subtypes e.g., α1β2γ2 and α6β2γ2, and subsequently attempted to determine which subunit(s) may be phosphorylated. Our results support the hypothesis that PTK phosphorylation may maintain GABAA receptor function. In addition, we suggest this tyrosine phosphorylation occurs at the γ2 subunit of the receptor.Item Modulation of Manganese Superoxide Dismutase by 17-Beta Estradiol(2008-05-01) Gottipati, Srinivas; Thomas YorioGottipati, Srinivas. Modulation of manganese superoxide dismutase activity by 17-beta estradiol. Master of Science (Cell Biology and Genetics), May, 2008. We have previously reported that 17β-Estradiol (17β-E2) can protect human lens epithelial cells against oxidative stress by preserving mitochondrial function, acting as a positive regulator of the MAPK signal transduction pathway. While pERK plays a significant role in stabilizing the inner mitochondrial membrane to maintain the mitochondrial membrane potential during oxidative stress, the protective mechanisms activated by 17β-E2 are probably multifactorial acting via both genomic and non genomic pathways. This study examined the effects of 17β-E2 on the expression and activity of MnSOD, which is present exclusively in the mitochondria, as a possible mechanism by which it affords protection against oxidative stress. Our results demonstrate that 17β-E2 rapidly increases the activity of MnSOD in a time dependent manner. This augmentation of activity of MnSOD by 17β-E2 is seen in the absence of a corresponding increase in the mRNA and protein expression, thereby which estrogens protect the cells against oxidative stress will help us in developing estrogens to be useful therapies for the prevention of cataract in postmenopausal women and non feminizing estrogens may provide similar protection in men.