Marc M. Greenberg

This study shows human pol δ holoenzymes can bypass various lesions with insertion and extension efficiencies ranging from 0 to 100%.

This study investigates how human DNA polymerase β processes the mutagenic lesion Fapy*dG during DNA replication, showing inefficient bypass and incorporation, suggesting mutagenicity arises from bypass rather than lesion incorporation.

The paper introduces a PAR photoaffinity probe to identify PAR-binding proteins, revealing novel binders and demonstrating length-selective PAR binding.