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Analysis of Epigenetic Alterations to Proprotein Convertase Genes in Disease

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Book cover Proprotein Convertases

Part of the book series: Methods in Molecular Biology ((MIMB,volume 768))

Abstract

Epigenetic alterations produce heritable changes in phenotype or gene expression without changing DNA sequence. Modified levels of gene expression contribute to a variety of human diseases encompassing genetic disorders, pediatric syndromes, autoimmune disease, aging, and cancer. Alterations in proprotein convertase gene expression are associated with numerous disease states; however, the underlying mechanism for changes in PC gene expression remains understudied. Epigenetic changes in gene expression profiles can be accomplished through modification of chromatin, specifically via chemical modification of DNA bases (methylation of cytosine) or associated histone proteins (acetylation or methylation). In general, active chromatin is associated with low DNA methylation status and histone acetylation, whereas silenced gene are typically in inactive regions of chromatin exhibiting DNA hypermethylation and histone deacetylation. This chapter will provide in-depth protocols to analyze epigenetic alterations in proprotein convertase gene expression using the PCSK6 gene in the context of human ovarian cancer as a model system.

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Acknowledgments

This work was supported by funds to MWN from the Canadian Institute of Health Research regional partnership grant program (ROP-91758) partnered with the Nova Scotia Health Research Foundation (MED-Matching-2008-4881) and the Dalhousie Cancer Research Program.

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Correspondence to YangXin Fu .

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Fu, Y., Nachtigal, M.W. (2011). Analysis of Epigenetic Alterations to Proprotein Convertase Genes in Disease. In: Mbikay, M., Seidah, N. (eds) Proprotein Convertases. Methods in Molecular Biology, vol 768. Humana Press. https://doi.org/10.1007/978-1-61779-204-5_12

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  • DOI: https://doi.org/10.1007/978-1-61779-204-5_12

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  • Publisher Name: Humana Press

  • Print ISBN: 978-1-61779-203-8

  • Online ISBN: 978-1-61779-204-5

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