Polymerase Theta-mediated DNA End-Joining Repair in the Maintenance of Genome Stability

Xiangyu Yan

doi:10.62051/rg3zk642

Authors

Xiangyu Yan

DOI:

https://doi.org/10.62051/rg3zk642

Keywords:

DNA double-strand break; Polymerase theta-meditated end-joining; BRCA-mutated breast cancer; DNA polymerase theta; DNA polymerase delta.

Abstract

The DNA double-strand break (DSB) always occurs within genome. The pathways that repair the DSB are essential in keeping cell viability. This review will focus on the recent understanding of TMEJ, especially two key protein factors involved in the TMEJ repair pathway², DNA polymerase theta (Polθ) and DNA polymerase delta (Polδ), and discuss the potential mechanism of choosing repair pathways when there is a DNA Double Strand Break. We dissect TMEJ's unique mechanism of action, including recognition of DNA ends, microhomology search, end pairing, and DNA synthesis, by focusing on the enzyme Polθ as the central player to understand the repair pathway choice. We also discuss how BRCA-mutated cancer uses the TMEJ repair pathway to facilitate breast cancer cells' growth³. This review aims to provide a comprehensive overview of TMEJ's cellular functions, regulatory mechanisms, and pivotal role in BRCA-mutated breast cancer.

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