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- W2165822588 startingPage "373" @default.
- W2165822588 abstract "Posttranslational modifications of histones, alterations in the recruitment and functions of non-histone proteins, DNA methylation, and changes in expression of noncoding RNAs contribute to current models of epigenetic regulation. Nuclear receptors (NRs) are a group of transcription factors that, through ligand-binding, act as sensors to changes in nutritional, environmental, developmental, pathophysiologic, and endocrine conditions and drive adaptive responses via gene regulation. One mechanism through which NRs direct gene expression is the assembly of transcription complexes with cofactors and coregulators that possess chromatin-modifying properties. Chromatin modifications can be transient or become part of the cellular memory and contribute to genomic imprinting. Because many food components bind to NRs, they can ultimately influence transcription of genes associated with biologic processes, such as inflammation, proliferation, apoptosis, and hormonal response, and alter the susceptibility to chronic diseases (e.g., cancer, diabetes, obesity). The objective of this review is to highlight how NRs influence epigenetic regulation and the relevance of dietary compound-NR interactions in human nutrition and for disease prevention and treatment. Identifying gene targets of unliganded and bound NRs may assist in the development of epigenetic maps for food components and dietary patterns. Progress in these areas may lead to the formulation of disease-prevention models based on epigenetic control by individual or associations of food ligands of NRs." @default.
- W2165822588 created "2016-06-24" @default.
- W2165822588 creator A5037982277 @default.
- W2165822588 creator A5044003397 @default.
- W2165822588 creator A5084037167 @default.
- W2165822588 date "2014-07-01" @default.
- W2165822588 modified "2023-09-29" @default.
- W2165822588 title "Nuclear Receptors and Epigenetic Regulation: Opportunities for Nutritional Targeting and Disease Prevention" @default.
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