Linda Chelico

This study identifies TMEJ as the main repair pathway for APOBEC3A-induced DSBs and shows Polθ inhibition causes synthetic lethality in cancer cells with APOBEC3A activity.

This study investigates how APOBEC3F and APOBEC3G interact to resist HIV-1 Vif-mediated degradation and shows subtype-specific differences in Vif activity against these enzymes.

The paper identifies novel protein and RNA interactions of APOBEC3 enzymes, revealing deamination-independent roles in RNA biology and cancer.

This study shows that APOBEC3G drives mutagenesis and clonal evolution in bladder cancer, contributing to mutational profiles in multiple cancer types.