Brian J. Lee

This study shows that catalytically inactive PARP1, not PARP2, is responsible for PARP inhibitor-induced hematological toxicity in mice.

The paper identifies programmed clonal expansion during V(D)J recombination as an ATM-dependent vulnerability causing preferential lymphocyte depletion and myeloid bias after DNA damage.

The paper shows PARG inhibition causes nuclear condensates that sequester PAR-binding repair proteins, leading to cytotoxicity and identifying PAR-binding factor loss as potential biomarkers for PARG-targeted therapy.

This study shows that astrocyte redox imbalance causes neuronal hypoactivity and affective behaviors in epilepsy, distinct from seizure mechanisms.

This study shows that primate-specific Ku adaptation suppresses Alu-mediated alternative splicing, maintaining transcriptomic integrity and linking Ku function to brain development and disease.

This study shows that XRCC1 facilitates PARP1-mediated recruitment of PARP2 to DNA damage sites through PAR binding and interaction with PARP2.

The paper shows Ku suppresses RNA-mediated innate immune responses in human cells, enabling primate-specific Alu element expansion by reducing dsRNA-induced inflammation.

The paper shows that inactive PARP2 causes Tp53-dependent lethal anemia by blocking replication-associated nick ligation in erythroblasts, explaining PARPi-induced hematological toxicities.

This study identifies the SAP domain of Ku70 as limiting KU lateral movement on DNA, with DNA-PKcs partially masking this function in NHEJ.

This study shows that catalytically inactive PARP1 causes embryonic lethality and genome instability in a dominant-negative manner, revealing its severe impact on normal tissues.

This study shows ATR kinase prevents replication resource exhaustion in early S phase, supporting normal cell proliferation by regulating origin firing.

This study identifies the miR-124-AMPAR pathway as a common mediator linking polygenic risks to shared behavioral changes in schizophrenia and bipolar disorder.