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Signal transduction and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Brendan Egan, Adam P. Sharples
The tight packaging of DNA in chromatin must be unravelled before a gene can be transcribed. The packaging and unpackaging of DNA are known as chromatin remodelling and histone modifications are key mechanisms in the regulation of this process. Mapping of packaged and unpackaged DNA on a genome-wide scale has revealed that histone tail modifications are cell-specific and mark genes, transcription start sites and stretches of regulatory DNA, via which gene expression is regulated (53). Indeed, signal transduction pathways modulate chromatin remodelling by methylating (CH3, methyl group), acetylating (CH3CO, acetyl group) and phosphorylating histone proteins, especially in the tail regions of histones H3 and H4 (19, 20). The enzymes that catalyse these modifications include histone methyltransferases and histone demethylases as well as histone acetyltransferases and HDACs. The resultant modifications are abbreviated stating first the histone number, second the amino acid which is modified and finally the type of modification (ac stands for acetylation, me1, me2, m3 for methylation, dimethylation and trimethylation, respectively). For example, H3K27me3 refers to the trimethylation of lysine 27 (K is the one-letter abbreviation for lysine) of histone 3.
Nucleic Acids as Therapeutic Targets and Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
The other important epigenetic mechanism is histone acetylation/deacetylation. The attraction of methyl-binding domain (MBD) proteins associated with histone deacetylases (HDACs) represents a more generalized effect, as the chromatin structure can be completely changed by these enzymes, profoundly affecting the expression of more than one gene. This process, known as chromatin remodeling, involves acetylation of the chromatin causing it to “open” and become more accessible to the necessary transcription factors, thus promoting gene expression. Conversely, gene silencing results from deacetylation of the histones, which causes the condensation of chromatin due to the positively charged lysine amino groups released interacting with the negatively charged DNA (Figure 5.108).
Role of Epigenetics in Immunity and Immune Response to Vaccination
Published in Mesut Karahan, Synthetic Peptide Vaccine Models, 2021
Covalent modifications are crucial for development where they regulate the differentiation of stem cells to different cell types with various functions (Teif et al. 2014). One of the best-studied examples of this effect is the differentiation of neural stem cells into oligodendrocytes through chromatin remodeling with histone methylation (Hallgrimsson and Hall 2011). There are two mechanisms for chromatin remodeling: 1) post translational modifications and 2) DNA methylation.
Epigenetic control of skin immunity
Published in Immunological Medicine, 2023
ATP-dependent chromatin remodeling complexes facilitate chromatin repositioning in a non-covalent manner by utilizing energy from the hydrolysis of ATP. Examples of chromatin repositioning include nucleosome sliding, unwrapping, histone removal, and nucleosome reorganization [13]. Each phenomenon is facilitated by different multi-subunit chromatin remodeling complexes, including switch/sucrose-non-fermenting (SWI/SNF), nucleosome remodeling deacetylase (Mi-2/NuRD), imitation switch (ISWI), and inositol requiring 80 (INO80) (Table 2) [14–17]. Chromatin dynamics induced by the ATP-dependent chromatin remodeling complexes affect the ability of the transcriptional machinery, including histone modifying enzymes and/or DNA-binding transcription factors, to access DNA and exert their functions. These complexes work in concert with their corresponding transcriptional machinery and are thus involved in both activation and repression of transcription [18,19].
Epigenetic regulation of T cell development
Published in International Reviews of Immunology, 2023
Avik Dutta, Harini Venkataganesh, Paul E. Love
Chromatin remodeling complexes modify chromatin structure by transiently dislocating DNA/nucleosome interaction with the help of energy from ATP hydrolysis. This process helps to reposition nucleosomes and thus increases the accessibility of specific genes to the transcriptional machinery [36]. There is also crosstalk between the ATP-dependent chromatin remodeling mechanism and covalent modifications. It has been found that some “readers” of histone modifications are themselves subunits of ATP-dependent chromatin remodeling complexes [37]. To date four ATP-dependent remodeler families have been well characterized. They are: SWI/SNF, ISWI, INO80 and CHD/NuRD/Mi-2 [36]. These families of proteins have higher affinity toward post-translationally modified nucleosomal histone-tail residues and have regulatory domains that can undergo various biochemical and epigenetic alterations [36].
Epigenetic changes involved in hydroquinone-induced mutations
Published in Toxin Reviews, 2021
Minjuan Zeng, Shaopeng Chen, Ke Zhang, Hairong Liang, Jie Bao, Yuting Chen, Shiheng Zhu, Wei Jiang, Hui Yang, Yixian Wei, Lihao Guo, Huanwen Tang
Chromatin remodeling is the dynamic modification of chromatin architecture and plays an important role in DNA repair and gene transcriptional regulation (Moore et al.2019). PARP-1, as a sensor of DNA damage, can regulate chromatin structure by interacting with ATP-dependent nucleosome remodeling enzymes, histones, and MeCP2 (Kraus and Hottiger 2013, Becker et al.2016). Compared to control cells, protein levels of PARP-1was upregulated in a dose-dependent manner in TK6 cells exposed 48 h to HQ (10, 20, and 40 μmol/L; Luo et al.2018). However, the expression of PARP-1 decreased to the lowest level within 3 h and then gradually increased in TK6 cells (treated with 10.0 μmol/L HQ for 1, 2, 3, 4, 5, and 6 h; Ling et al.2016). Caruso et al. (2018) showed that PARP-1 and PARylation are important regulators of EZH2 function and lead to decreased EZH2-mediated heterochromatin formation, increasing the reading and transcription of genes. Gui et al. (2019) reported that PARP-1 promotes expression of the tumor activator, miR-155, via upregulation of MBD2, a member of the same family as MeCP2, in TK6 cells exposed to HQ. Luo et al. (2018) speculated that overexpression of the tumor suppressor miR-7-5p suppresses cell proliferation and promotes apoptosis by inhibiting the DNA damage repair mediated via PARP-1 and BRCA1 in TK6 cells exposed to HQ.