(2) Modification of histones by methylation or acetylation changes the accessibility of DNA at the site of these nucleosomes.
DNA methylation, post-translational modification of histones and chromatin remodeling are nuclear mechanisms implicated in epigenetic control of gene expression.
Covalent modification of histones with methylation or acetylation will result in the chromatin structural change and could be used as markers for chromatin structure.
In summary, the findings suggest that UHRF2 mediated the post-translational modification of histones and the initiation and progression of cancer.
This includes direct modification of nucleic acids (i.e. 5mC, 6mA, m6A, and pseudouridine), and post-translational modification of histones (e.g. methylation, and acetylation) [77, 78].
Post-translational modification of histones, ATP-dependent chromatin remodeling, and DNA methylation are interconnected nuclear mechanisms that ultimately lead to the changes in chromatin structure necessary to carry out epigenetic gene expression control.
In addition, the cell has evolved several interdependent processes capable of enhancing the accessibility of excision repair enzymes to DNA lesions in nucleosomes, including post-translational modification of histones, ATP-dependent chromatin remodeling and interchange of histone variants in nucleosomes.
Esteller joined CNIO in 2001, using the opportunity to pursue a then relatively unknown area of cancer epigenetics: the chemical modification of histones, nuclear proteins that package DNA and regulate gene expression.
Modification of histones and associated induction of heterochromatin formation serves to downregulate genes pre-transcriptionally; this process is referred to as RNA-induced transcriptional silencing (RITS), and is carried out by a complex of proteins called the RITS complex.
It has also been demonstrated that post-translational modification of histones can control gene activity.
Post-translational modification of histones by regulating cellular gene expression plays a critical role in sustained CpG island methylation [16].
