Ubiquitylation - Dependent Signaling in Heart Disease

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Translational Cardiology

Abstract

The regulation of cell signaling by posttranslational phosphorylation of proteins has emerged as a major mechanism by which external ligands regulate cell function. Like phosphorylation, modifying proteins with ubiquitin can regulate a number of ever-expanding cellular functions such as cell growth, apoptosis, the innate immune response, and proteins that regulate responses to DNA damage. In this chapter we review recently published findings implicating the ubiquitin proteasome system (UPS) in regulating key signal transduction pathways and transcription factors in the heart, including MAPK JNK, calcineurin, FOXO, p53, estrogen receptors α and β, NF-κB, and SMAD. We then discuss how regulation of these signal transduction pathways by the UPS plays a role in common cardiac diseases, including cardiac hypertrophy, heart failure, ischemia reperfusion injury, myocardial infarction, and diabetes.

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Acknowledgments

The authors’ laboratories and training are supported by the National Institutes of Health (R01HL104129 to M.W., R37HL065619 to C.P., T32HL069768 to W.H.D.T.T.).

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Correspondence to Monte S. Willis .

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Willis, M.S., Portbury, A., Ronnebaum, S., Zungu, M., Townley-Tilson, W.H.D., Patterson, C. (2012). Ubiquitylation - Dependent Signaling in Heart Disease. In: Patterson, C., Willis, M. (eds) Translational Cardiology. Molecular and Translational Medicine. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-61779-891-7_8

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