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Epigenetics is an essential mechanism to control gene expression and fundamental cellular processes. DNA methylation in CpG-rich promoters correlates with gene silencing. Histone modification including histone acetylation and deacetylation determines the stability of the chromatin structure. Condensed chromatin (heterochromatin), which has a higher-order histone-DNA structure, prevents the access of transcriptional activators to their target genes. The fundamental unit of eukaryotic chromatin consists of 146 bp of DNA wrapped around a histone octamer. Posttranslational modifications of the histone tail and the chromatin remodeling complex disrupt histone-DNA contacts and induce nucleosome mobilization. Histone acetylation of specific lysine residues in the histone tail plays a crucial role in epigenetic regulation. Histone acetylation is a dynamic process regulated by the antagonistic actions of 2 families of enzymes - the histone acetyltransferases (HATs) and the histone deacetylases (HDACs). The balance between histone acetylation and deacetylation serves as a key epigenetic mechanism for transcription factor-dependent gene expression and the developmental process. We review emerging evidence that DNA methylation, histone acetylation modified by HAT and/or HDAC, and transcription factor-associated molecules contribute to a mechanism that can alter chromatin structure, gene expression, and cellular differentiation during chondrogenesis.
収録刊行物
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- Acta Medica Okayama
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Acta Medica Okayama 64 (3), 155-161, 2010-06
Okayama University Medical School
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詳細情報 詳細情報について
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- CRID
- 1390853649535581824
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- NII論文ID
- 120002311043
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- NII書誌ID
- AA00508441
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- ISSN
- 0386300X
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- PubMed
- 20596126
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- IRDB
- PubMed
- CiNii Articles