Daniel Durocher

This study identifies SLC25A28 as a synthetic lethal target in NER-deficient cancers, showing its loss impairs cell viability and increases oxidative stress.

The paper identifies DDIAS as a DNA-binding effector of the CIP2A-TOPBP1 complex that suppresses single-stranded DNA during mitosis, protecting genome integrity and interacting genetically with DNA polymerase.

This study identifies synthetic lethal interactions between cancer drivers and tractable targets using CRISPR screens and cancer dependency data, offering new drug targets for therapy.

This study shows WEE1 inhibitors trigger the integrated stress response via GCN2 activation, leading to translational shutdown, which can be mitigated by low-dose or combination treatments.

This paper develops PCIP-1, a PARP-based chemical inducer of proximity that rewires DNA repair by recruiting BET proteins to PARP2, showing synthetic lethality in cancer cells with homologous recombination deficiencies.

The paper identifies a synthetic lethal relationship between SMARCAL1 and FANCM, showing their combined loss causes severe genome instability due to chromosome breakage at simple repeat regions.

The paper identifies NFATC2IP as a mediator of SUMO-dependent genome integrity through CRISPR/Cas9 screens and functional validation.

The paper uses AlphaFold2 to predict structural interactions in the 53BP1 pathway, identifying a novel RIF1-SHLD3 binding interface critical for DNA repair.

The paper identifies 160 genes that suppress DNA damage in human cells through CRISPR/Cas9 screens, highlighting GNB1L's role in ATR biogenesis and its link to neuropsychiatric disorders.

This study identifies RIF1 as a phosphopeptide-binding protein that interacts with phosphorylated 53BP1 epitopes to facilitate DNA repair and modulate shieldin recruitment.

This study identifies two redundant ubiquitin-dependent pathways for BRCA1 localization to DNA damage sites, involving RAP80 and the BRCA1 RING domain.

The paper identifies a consensus set of 117 genes that promote survival when ATR kinase activity is suppressed, validated through CRISPR/Cas9 screens and including previously unknown modulators of ATR inhibitor response.

drugZ identifies chemogenetic interactions from CRISPR screens, finding more homologous recombination repair pathway genes and confirming KEAP1 loss as a resistance factor for ERK inhibitors.

The paper introduces BFG-GI to map DNA damage-dependent genetic interactions in yeast by combining party mating and barcode fusion genetics, revealing new condition-specific interactions.

The paper evaluates CRISPR/Cas9 knockout screens in human cell lines and designs an optimized gRNA library to improve gene knockout efficiency and accuracy.

This paper develops a genetically encoded inhibitor of 53BP1, i53, which enhances homology-based gene editing by blocking NHEJ and promoting HR in non-replicating cells.