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Titlebook: Epigenetics in Cardiac Disease; Johannes Backs,Timothy A. McKinsey Book 2016 Springer International Publishing Switzerland 2016 Cardiac de

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楼主: 欺侮
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Book 2016 will stimulate further research in this exciting field. Edited and written by internationally respected experts, it addresses the needs of professors, students and researchers working in the fields of cardiac biology and epigenetics..
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American Protestants and TV in the 1950s, some of which is a component of the nuclear matrix, a dynamic RNA protein nuclear sub-structure. Non-coding RNA and coding RNA are associated with epigenetic modifiers, architectural chromatin proteins, coactivators and corepressors. The impact of changes in DNA sequence (single nucleotide polymorphisms) on the epigenome is discussed.
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Palgrave Studies in the History of the Mediart development. Heart development is orchestrated by complicated biological processes, including signal transduction, transcriptional regulation, and epigenetic regulation. In this chapter, we review the current processes of epigenetic modifications during heart development.
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SVOD: A Place for (Outer) Space?ng of autophagic components. Autophagy has been implicated in cardiac hypertrophy, heart failure, ischemia/reperfusion injury, anticancer drug-induced cardiomyopathy and glycogen storage diseases. Manipulations of autophagy by HDAC inhibition is a novel strategy worthy of consideration in the treatment of these common cardiovascular diseases.
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Book 2016sms. Further, it discusses the roles of chromatin modifications (in particular DNA methylation and histone modifications) and of chromatin regulators in the context of cardiac diseases. The book provides readers with an overview of our current understanding of epigenetic regulation in the heart, and
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https://doi.org/10.1057/9780230612518 enzymes, histone deacetylases (HDACs), represent such nodal points. We discuss recent findings that illustrate how HDACs not only control cardiac gene expression via epigenetic regulation, but also serve crucial non-genomic functions in the heart through deacetylation of non-histone proteins.
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