Area of research
Molecular Biology · Oncology
Research interest
Research interests include DNA Repair Mechanisms, CRISPR and Genetic Engineering, Ubiquitin and proteasome pathways, and Genomics and Chromatin Dynamics.
Design of a Targeted Covalent Probe to Interrogate the DNA Polymerase Activity of Polθ.
CRISPR-enabled genetic screens identify synthetic lethal targets across frequently altered cancer drivers
Synthetic lethal strategies for the development of cancer therapeutics.
Rewiring DNA repair with PARP-based chemical inducers of proximity
WEE1 inhibitors trigger GCN2-mediated activation of the integrated stress response
Mitotic single-stranded DNA suppression by DDIAS
Author Correction: PP4 is a γH2AX phosphatase required for recovery from the DNA damage checkpoint.
Author Correction: A substrate binding model for the KEOPS tRNA modifying complex.
WEE1 inhibitors trigger GCN2-mediated activation of the integrated stress response.
Author Correction: A substrate binding model for the KEOPS tRNA modifying complex
Synthetic lethal strategies for the development of cancer therapeutics
Genome-wide CRISPR screens identify novel regulators of wild-type and mutant p53 stability.
Profound synthetic lethality between SMARCAL1 and FANCM
NFATC2IP is a mediator of SUMO-dependent genome integrity.
Profound synthetic lethality between SMARCAL1 and FANCM
An AlphaFold2 map of the 53BP1 pathway identifies a direct SHLD3-RIF1 interaction critical for shieldin activity.
Functional characterization of C21ORF2 association with the NEK1 kinase mutated in human in diseases
Genome-scale mapping of DNA damage suppressors through phenotypic CRISPR-Cas9 screens.
Functional characterization of C21ORF2 association with the NEK1 kinase mutated in human in diseases.
A mitotic glue for shattered chromosomes.
An AlphaFold2 map of the 53BP1 pathway identifies a direct SHLD3-RIF1 interaction critical for DNA repair activity
Chemogenetic profiling of ubiquitin-like modifier pathways identifies NFATC2IP as a mediator of SUMO-dependent genome integrity
CCNE1 amplification is synthetic lethal with PKMYT1 kinase inhibition.
The CIP2A-TOPBP1 complex safeguards chromosomal stability during mitosis.
RIF1 acts in DNA repair through phosphopeptide recognition of 53BP1
Global cellular response to chemical perturbation of PLK4 activity and abnormal centrosome number.
Genome-wide CRISPR screens identify novel regulators of wild-type and mutant p53 stability
Interaction with C21ORF2 controls the cellular functioning of the NEK1 kinase
Author Reply to Peer Reviews of Genome-wide CRISPR screens identify novel regulators of wild-type and mutant p53 stability
Genome-scale mapping of DNA damage suppressors identifies GNB1L as essential for ATM and ATR biogenesis