Keith W. Caldecott

This study shows that DNA polymerase beta suppresses excessive PARP1 engagement during DNA base excision repair, enabling efficient repair and preventing transcriptional suppression.

The paper shows that parp1 deletion rescues cerebellar hypotrophy in xrcc1 mutant zebrafish, suggesting PARP1 inhibition could be therapeutic for neurological disorders.

The paper compares DNA combing and spreading techniques to determine their ability to resolve sister chromatids during DNA replication, finding that DNA combing can detect strand-specific alterations while DNA spreading cannot.

This paper shows that the SARS-CoV-2 Nsp3 macrodomain reverses PARP9/DTX3L-dependent ADP-ribosylation induced by interferon signaling in human cells.

The paper identifies DNA single-strand breaks (SSBs) accumulating at neuronal enhancers and shows their repair involves PARP1, XRCC1, and DNA polymerase β.

This study shows that aberrant PARP1 activity at unrepaired DNA breaks causes deregulated presynaptic calcium signaling and lethal seizures in Xrcc1-defective mice, suggesting PARP inhibition as a therapeutic strategy.