| Issue |
BIO Web Conf.
Volume 100, 2024
International Scientific Forum “Modern Trends in Sustainable Development of Biological Sciences” (IFBioScFU 2024)
|
|
|---|---|---|
| Article Number | 03010 | |
| Number of page(s) | 9 | |
| Section | Fundamental and Applied Research in Genetics and Molecular Biology | |
| DOI | https://doi.org/10.1051/bioconf/202410003010 | |
| Published online | 08 April 2024 | |
Putative Role of the Futile Repair Initiated by Human Thymine-DNA Glycosylase in Formation of Programmed Strand Breaks in Neuronal Enhancers
1 Laboratory of DNA Repair and Carcinogenesis Mechanisms, UMR 9019 CNRS, Gustave Roussy Cancer Campus, Villejuif, 94800, France
2 SRI of Biology and Biotechnology Problems, al-Farabi Kazakh National University, Almaty, 050040, Kazakhstan
* Corresponding author: manatkyzy.diana@gmail.com
Enhancers are regulatory DNA elements that play a crucial role in controlling gene expression in specific cell types, including neurons. Enhancer activity is tightly regulated and involves the recruitment of various proteins and enzymes to facilitate the opening of chromatin and the activation of target genes. Given the importance of enhancers in neuronal function, the presence of single-strand DNA breaks (SSBs) in these regions raises intriguing questions about their potential impact on gene regulation and neuronal activity. Single-strand DNA breaks (SSBs) have been identified as important lesions in the genome, with the potential to influence gene expression and genomic stability. By understanding the role of SSB repair and human mono-functional Thymine-DNA glycosylase (TDG) catalyzed futile excision of regular bases in enhancer regions, we may gain insights into the molecular mechanisms underlying neurological disorders and potentially identify new therapeutic targets for intervention.
© The Authors, published by EDP Sciences, 2024
This is an Open Access article distributed under the terms of the Creative Commons Attribution License 4.0, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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