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Utilizing Protein Phosphatase Inhibitors to Define PP2A as a Regulator of Ataxia-Telangiectasia Mutated

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Protein Phosphatase Protocols

Part of the book series: Methods in Molecular Biology ((MIMB,volume 365))

Abstract

Ataxia-telangiectasia mutated (ATM) is a serine/threonine protein kinase that plays a central role in controlling the cellular response to DNA double-strand breaks caused by ionizing radiation. Ionizing radiation induces the autophosphorylation of ATM on serine 1981; however, the precise mechanisms that regulate ATM autophosphorylation are not fully understood. By treating cells with okadaic acid, a cell-permeable protein phosphatase inhibitor, together with assays to quantify the activity of particular protein phosphatases, we have demonstrated that the autophosphorylation of ATM on serine 1981 is regulated by a protein phosphatase 2A-like activity. Here, we describe the series of experiments that employed protein phosphatase inhibitors to establish that ATM was regulated by a type-2A protein phosphatase.

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References

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© 2007 Humana Press Inc.

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Goodarzi, A.A., Douglas, P., Moorhead, G.B.G., Lees-Miller, S.P. (2007). Utilizing Protein Phosphatase Inhibitors to Define PP2A as a Regulator of Ataxia-Telangiectasia Mutated. In: Moorhead, G. (eds) Protein Phosphatase Protocols. Methods in Molecular Biology, vol 365. Springer, Totowa, NJ. https://doi.org/10.1385/1-59745-267-X:47

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  • DOI: https://doi.org/10.1385/1-59745-267-X:47

  • Publisher Name: Springer, Totowa, NJ

  • Print ISBN: 978-1-58829-711-2

  • Online ISBN: 978-1-59745-267-0

  • eBook Packages: Springer Protocols

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