Linking the DNA repair template to the Cas9 ribonucleoprotein complex enhances homology-directed repair of the induced DNA double strand break.

Multiple solution-state structures are used for the DNA double-strand break repair functions of the Mre11-Rad50 protein complex.

Transcription factor proteins play an important role in modulating base damage formation and excision repair at the binding sites in the genome.

Unbiased proteomics and molecular analysis revealed a new role for S6K1 in regulating DNA repair through the orchestrated phosphorylation of CDK1 and MSH6. The findings may explain why RPS6KB1 gene amplification contributed to breast cancer drug resistance.

Kinesin Kif2C is recruited to DNA damage sites, modulates the mobility and dynamics of DNA damage foci, and promotes DNA double strand break repair.

The repair of spontaneous DNA damage can introduce mutators that lead to further genetic changes, which could underlie evolutionary change, disease and aging.

Polyglutamine expansion in mutant huntingtin disrupts a novel transcription-coupled DNA repair complex, providing an undescribed mechanism of neuronal toxicity and degeneration in Huntington's disease.

Biochemical studies revealed novel property of human tumor suppressor PALB2, which significantly contribute into DNA repair in cells and can be targeted for the development of novel anticancer treatment.

Experiments on E. coli show that multiple mechanisms contribute to extreme resistance to ionizing radiation in bacteria, with mutations to three genes for DNA repair having a prominent role in one evolved population.

Biochemical analysis shows that muscle-invasive-bladder-cancer cells are deficient in DNA repair and hypermutable, non-muscle-invasive-bladder-cancer cells are proficient in DNA repair, DNA repair capacity is regulated by tumor suppressor TAp63g, and cell invasions are regulated by TAp63g and p53.