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Calpain 2 regulates proteolysis of Akt in glioblastoma cell invasion Public Deposited

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  • Glioblastoma multiforme is a form of primary brain cancer in humans with a 5 year survival rate of less than 4%. Glioblastoma cells are characterized by their highly invasive nature linked to mutations in key signaling proteins such as PTEN, resulting in loss of expression of this lipid phosphatase. When PTEN is not expressed, the phosphorylation and dephosphorylation equilibrium is disturbed resulting in elevated phosphatidylinositol 3,4,5-trisphosphate (PIP3) levels in the cell and constitutive activation of Akt. The Akt pathway, downstream of phosphoinositide 3-kinase production of PIP3, is known to be highly activated and involved in the progression of glioblastoma. Akt is activated by phosphorylation on Thr308 and Ser473 sites in a PIP3-dependent manner. We are examining calpain 2 proteolysis as a novel mechanism for modulating the activity of Akt. Understanding the regulation Akt may lead to new approaches for controlling the activity of a key promoter of cancer progression.
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  • This research was supported through a research grant by the Oregon State University (OSU) general research fund to J.A.G., grants from the Howard Hughes Medical Institute (HHMI), Undergraduate Research, Innovation, Scholarship and Creativity (URISC), and Cripps Undergraduate Research (CURe) to M.N.
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