DNA repair genomic stability homologous recombination non-homologous end joining CRISPR-Cas9 cell cycle regulation

DNA repair mechanisms are vital for maintaining genomic stability and preventing mutations that can lead to diseases such as cancer. This study aims to elucidate the complex network of DNA repair pathways in eukaryotic cells, focusing on the repair of double-strand breaks. Using advanced molecular biology techniques, including CRISPR-Cas9 gene editing and next-generation sequencing, we investigated the roles of key proteins involved in homologous recombination and non-homologous end joining. Our findings reveal novel interactions between repair proteins and suggest a regulatory mechanism that controls pathway choice based on cell cycle stage and DNA damage context. We identified that certain post-translational modifications of repair proteins enhance their activity, offering potential targets for therapeutic intervention. In conclusion, this research advances our understanding of DNA repair processes and suggests new avenues for enhancing genome stability in medical and biotechnological applications.

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