Multi-level regulation of CtIP, BRCA1, and RAD51 expression: From transcription to post-translational modification

Abstract

Homologous recombination (HR) is a high-fidelity DNA double-strand break repair pathway that plays a central role in preserving genome stability and suppressing tumorigenesis. Core HR proteins, including CtIP, BRCA1, and RAD51, function in a tightly coordinated manner to mediate DNA end resection, pathway choice, and homology-directed strand exchange. Increasing evidence indicates that the abundance, activity, and chromatin engagement of these HR regulators are not constitutive but are dynamically controlled across multiple regulatory layers, including transcriptional programs, post-transcriptional RNA regulation, and post-translational proteostasis mechanisms. These regulatory systems integrate cell-cycle, stress signaling, and metabolic context to regulate HR capacity. In this review, we present an integrated framework describing how CtIP, BRCA1, and RAD51 are regulated across transcriptional, post-transcriptional, and post-translational levels, with an emphasis on mechanisms that jointly control multiple HR proteins as well as gene-specific regulatory modules.

Keywords

Homologous recombination / CtIP / BRCA1 / RAD51 / post-translational regulation

1 Acknowledgements

ChatGPT was used solely for language polishing during the manuscript preparation process. All research content, including study design, interpretations, and figures, is original and was not generated using AI tools. The authors take full responsibility for the integrity, originality, and accuracy of the work.

2 Authors contribution

Chung Y, Kim M, Jeong S, Amarsanaa E: Conceptualization, methodology, writing-original draft, writing-review & editing.

Lee Y, Myung K: Conceptualization, methodology, writing-review & editing.

3 Conflicts of interest

The authors declare no conflicts of interest.

4 Ethical approval

Not applicable.

5 Consent to participate

Not applicable.

6 Consent for publication

Not applicable.

7 Availability of data and materials

Not applicable.

Funding

This work was supported by the Institute for Basic Science (Grant No. IBS-R022-D1).

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