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The rate of DNA unwinding by RecQ helicases is dramatically modulated by the DNA duplex stability in a geometry-dependent manner, providing an intrinsic mechanism for suppressing illegitimate recombination.

Socio-economic hierarchies may be bad for health, even among people living in a relatively traditional, small-scale society in the Bolivian Amazon.

Targeting Werner syndrome helicase might constitute a novel opportunity for the treatment of a clinically defined subset of patients harboring MSI-H/MMR-deficient tumors.

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.

DNA lesions formed by alkylating agents trigger double-strand breaks, in the absence of replication, by the action of MMR and BER at nearby O-alkyl and N-alkyl adducts, respectively.

Exosomes secreted from pancreatic cancer cells can function as a classic initiator in the multi-step cellular transformation process.

Polymerase θ is among the most proficient terminal transferases known and switches between three different mechanisms of terminal transferase activity.

Biophysical modeling, performed in silico, can predict the abundance, metabolic stability, and function of MLH1 inside living cells.

A structural investigation reveals details of the mechanism by which the nuclease RecJ processes DNA ends to repair double strand breaks.