Histone methylation versus histone acetylation: new insights into epigenetic regulation

Rice, Judd C.; Allis, C. David

doi:10.1016/s0955-0674(00)00208-8

Cited by 617 publications

(457 citation statements)

References 97 publications

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“…For instance, acetylation of specific residues in histone H3 and H4 is associated with an open chromatin configuration and gene transcription. In contrast, deacetylation of these residues is associated with a repressive state (Rice and Allis, 2001). Consequently, combinations of histone deacetylase inhibitors with hypomethylating agents results in reactivation of gene expression (Richon and O'Brien, 2002), cell cycle arrest and apoptosis (Zhu et al, 2001b;Tang et al, 2004;Schmelz et al, 2005;Walton et al, 2008).…”

Section: Cell Death Signalingmentioning

confidence: 99%

Nucleoside analogs: molecular mechanisms signaling cell death

2008

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Nucleoside analogs are structurally similar antimetabolites that have a broad range of action and are clinically active in both solid tumors and hematological malignancies. Many of these agents are incorporated into DNA by polymerases during normal DNA synthesis, an action that blocks further extension of the nascent strand and causes stalling of replication forks. The molecular mechanisms that sense stalled replication forks activate cell cycle checkpoints and DNA repair processes, which may contribute to drug resistance. When replication forks are not stabilized by these molecules or when subsequent DNA repair processes are overwhelmed, apoptosis is initiated either by these same DNA damage sensors or by alternative mechanisms. Recently, strategies aimed at targeting DNA damage checkpoints or DNA repair processes have demonstrated effectiveness in sensitizing cells to nucleoside analogs, thus offering a means to elude drug resistance. In addition to their DNA synthesisdirected actions many nucleoside analogs trigger apoptosis by unique mechanisms, such as causing epigenetic modifications or by direct activation of the apoptosome. A review of the cellular and molecular responses to clinically relevant agents provides an understanding of the mechanisms that cause apoptosis and may provide rationale for the development of novel therapeutic strategies.

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Section: Cell Death Signalingmentioning

confidence: 99%

Nucleoside analogs: molecular mechanisms signaling cell death

2008

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“…Each of the core histones can be modified at several amino acids and for each amino acid more than one type of posttranslation modification is possible 3,4 . For example, histone H3 is known to be modified at 425 amino acids, and several lysines in histone H3 are known to be acetylated or methylated [5][6][7] . This variety of histone modifications and their correlation with gene activity forms the basis of the histone code 8 .…”

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confidence: 99%

Mycobacteria modulate host epigenetic machinery by Rv1988 methylation of a non-tail arginine of histone H3

et al. 2015

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“…As a result, histones are deacetylated and gene transcription is most often repressed. It has also been suggested that DNA methylation could lead to gene silencing by MBD proteins that recruit HMTs, which methylate lysine 9 in histone H3 and subsequently repress gene transcription ( Figure 2C) (reviewed in Rice and Allis, 2001;Brown and Strathdee, 2002).…”

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confidence: 99%

Linking the epigenetic ‘language’ of covalent histone modifications to cancer

2004

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Covalent modifications of histones, such as acetylation, methylation, and phosphorylation, and other epigenetic modulations of the chromatin, such as methylation of DNA and ATP-dependent chromatin reorganisation, can play a major part in the multistep process of carcinogenesis, with far-reaching implications for human biology and human health. This review focuses on how aberrant covalent histone modifications may contribute to the development of a variety of human cancers, and discusses the recent findings with regard to potential therapies.

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Histone methylation versus histone acetylation: new insights into epigenetic regulation

Cited by 617 publications

References 97 publications

Nucleoside analogs: molecular mechanisms signaling cell death

Nucleoside analogs: molecular mechanisms signaling cell death

Mycobacteria modulate host epigenetic machinery by Rv1988 methylation of a non-tail arginine of histone H3

Linking the epigenetic ‘language’ of covalent histone modifications to cancer

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