The hypothesis for the research study was “The connection of p53 activity and p53 Ser18 phosphorylation to metabolic regulation supports a model whereby the mechanism of ATM-mediated physiological regulation of insulin sensitivity may involve p53 activity and ATM-mediated p53 phosphorylation” (Heather, Armata, Golebiowski, Young, Jin Ko, Jason, Kim, and Sluss 3). To test the above hypothesis the metabolic control in mice was compared in presence and absence of a germ line mutation in p53 phosphorylation site Ser18. These p53 mice shows defects in p53-mediated apoptosis and gene expression (Heather 10), but unlike p53-null mice, p53 mice cultivate tumors lone at ...
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