DNA double-strand break (DSB) repair pathway choice is governed by the opposing activities
of 53BP1 and BRCA1. 53BP1 stimulates nonhomologous end joining (NHEJ), whereas …

53BP1 (also called TP53BP1) is a chromatin-associated factor that promotes immunoglobulin
class switching and DNA double-strand-break (DSB) repair by non-homologous end …

Mitotic cells inactivate DNA double-strand break (DSB) repair, but the rationale behind this
suppression remains unknown. Here, we unravel how mitosis blocks DSB repair and …

The NuA4/TIP60 acetyltransferase complex is a key regulator of genome expression and
stability. Here we identified MBTD1 as a stable subunit of the complex, and we reveal that, via a …

Programmable nucleases, such as Cas9, are used for precise genome editing by homology-dependent
repair (HDR) 1 , 2 , 3 . However, HDR efficiency is constrained by competition …

DNA double-strand breaks (DSBs) elicit a histone modification cascade that controls DNA
repair 1 , 2 , 3 . This pathway involves the sequential ubiquitination of histones H1 and H2A by …

The response to DNA double-strand breaks (DSBs) entails the hierarchical recruitment of
proteins orchestrated by ATM-dependent phosphorylation and RNF8-mediated chromatin …

… We are grateful to past and present members of the Weitzman and Fradet-Turcotte labs and
… Work on viruses and DNA repair in the Fradet-Turcotte lab has been supported by a grant …

Replication of the papillomavirus genome is initiated by the assembly of a complex between
the viral E1 and E2 proteins at the origin. The E1 helicase is comprised of a C-terminal …

The ability to perturb genes in human cells is crucial for elucidating gene function and holds
great potential for finding therapeutic targets for diseases such as cancer. To extend the …