Oxidative Stress Key Research Data and Analysis

1126 Words Feb 3rd, 2018 5 Pages
When Wild type and GAL7::IPC1 strains were exposed to galactose and glucose, DAG (activator of PKC1) levels in the GAL7::IPC1 strain increased when IPC1 was induced by galactose, and decreased when IPC1 was repressed by glucose. Furthermore, phytoceramide levels were increased when IPC1 was down regulated by glucose in the GAL7::IPC1 strain. In both wild type strains, no change was seen when IPC1 was up or down regulated, as expected (Fig. 2).
PKC1 activity in relation to DAG and Phytoceramide exposure. Since IPC1 regulates DAG and phytoceramide levels, the authors wanted to explore if DAG or phytoceramide can control PKC1 activity. DAG or phytoceramide were delivered in Triton x-100 lipid micelles and histone phosphorylation by recombinant PKC1 was measured in absence or presence of lipids. Without lipids, Pkc1 activity was 31.5 pmol/min/mg. When DAG subspecies were added, Pkc1 activity increased up to two fold (Fig. 3A). In order to make sure kinase activity measured was specific to Pkc1, APP1 activity was measured when exposed to DAG subspecies and as expected, did not cause phosphorylation of histone, which was expected (Fig. 3B). When phytoceramide lipids were added, Pkc1 activity decreased by about 50% compared to no phytoceramide, which was expected because phtyoceramide is an inhibitor of Pkc1 (Fig. 3C).

Study 2:…
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