Area of research
Molecular Biology · Oncology
Research interest
Research interests include DNA Repair Mechanisms, CRISPR and Genetic Engineering, Genomics and Chromatin Dynamics, and Cancer-related Molecular Pathways.
Genome-wide analysis of DNA-PK-bound MRN cleavage products supports a sequential model of DSB repair pathway choice
DNA-dependent protein kinase promotes DNA end processing by MRN and CtIP
ATM and PRDM9 regulate SPO11-bound recombination intermediates during meiosis
The ARK Assay Is a Sensitive and Versatile Method for the Global Detection of DNA-Protein Crosslinks
RPA Phosphorylation Inhibits DNA Resection
RNA–DNA hybrids and the convergence with DNA repair
Purification and Biophysical Characterization of the Mre11-Rad50-Nbs1 Complex
20 Years of Mre11 Biology: No End in Sight
ATM directs DNA damage responses and proteostasis via genetically separable pathways
MRI Is a DNA Damage Response Adaptor during Classical Non-homologous End Joining
Targeting p38α Increases DNA Damage, Chromosome Instability, and the Anti-tumoral Response to Taxanes in Breast Cancer Cells
Mitochondrial redox sensing by the kinase ATM maintains cellular antioxidant capacity
Sae2/CtIP prevents R-loop accumulation in eukaryotic cells
Homeodomain Proteins Directly Regulate ATM Kinase Activity
Single-Molecule Imaging Reveals How Mre11-Rad50-Nbs1 Initiates DNA Break Repair
Rad50 ATPase activity is regulated by DNA ends and requires coordination of both active sites
Genetic Separation of Sae2 Nuclease Activity from Mre11 Nuclease Functions in Budding Yeast
The Conserved ATM Kinase RAG2-S365 Phosphorylation Site Limits Cleavage Events in Individual Cells Independent of Any Repair Defect
Mre11 Is Essential for the Removal of Lethal Topoisomerase 2 Covalent Cleavage Complexes
Nbs1 Converts the Human Mre11/Rad50 Nuclease Complex into an Endo/Exonuclease Machine Specific for Protein-DNA Adducts
Regulation of the DNA Damage Response by DNA-PKcs Inhibitory Phosphorylation of ATM
Single-molecule imaging reveals the mechanism of Exo1 regulation by single-stranded DNA binding proteins
EXD2 promotes homologous recombination by facilitating DNA end resection
Mechanisms of ATM Activation
ATM functions at the peroxisome to induce pexophagy in response to ROS
CtIP: A DNA damage response protein at the intersection of DNA metabolism
BRCA1 and CtIP Are Both Required to Recruit Dna2 at Double-Strand Breaks in Homologous Recombination
Sumoylation Influences DNA Break Repair Partly by Increasing the Solubility of a Conserved End Resection Protein
Direct measurement of single-stranded DNA intermediates in mammalian cells by quantitative polymerase chain reaction
Catalytic and Noncatalytic Roles of the CtIP Endonuclease in Double-Strand Break End Resection