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- W2743606947 abstract "Abstract Within the human body, nitric oxide (NO) can arise from several sources including enzymatic synthesis, dietary nitrate, and pharmacological agents. Regardless of its source, the phenotypic consequences of NO production are influenced by complex microenvironmental factors that determine the target molecules NO will react with. Classical signaling mechanisms of NO are mediated via interactions with soluble guanylyl cyclase (sGC) and other heme-containing proteins or through the formation of protein adducts (S-nitrosothiols, 3-nitrotyrosine, and dinitrosyliron complexes). These interactions usually result in a loss or gain of protein function, thereby altering cellular phenotype. In addition, multiple lines of evidence have emerged recently demonstrating that a significant proportion of phenotypic changes attributed to NO production may be downstream from epigenetic regulatory events. It is becoming clear that NO affects dozens of histone modifications as well as DNA adducts, thus altering the epigenetic programs controlling the gene expression patterns that dictate cell phenotype, fate, and differentiation. This chapter will give an overview of the major NO-driven epigenetic mechanisms using specific examples." @default.
- W2743606947 created "2017-08-17" @default.
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- W2743606947 date "2017-01-01" @default.
- W2743606947 modified "2023-10-18" @default.
- W2743606947 title "Mechanisms of Epigenetic Regulation by Nitric Oxide" @default.
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- W2743606947 doi "https://doi.org/10.1016/b978-0-12-804273-1.00020-x" @default.
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