Stephen P. Jackson

This study identifies PRD mutants of ATM that are constitutively active, showing increased phosphorylation of targets without requiring MRN/DNA, and suggests potential for small-molecule modulators.

The paper identifies SP110 as a negative regulator of type 1 interferon-driven cell death by counteracting SP100's toxic filament formation through CARD domain interactions.

The paper identifies MAEA as a critical regulator of DNA repair and replication, with loss of function causing developmental delay and neurodevelopmental deficits.

The paper develops scOUT-seq to profile DNA repair outcomes in single cells and finds that repair outcomes vary significantly across cell types and subtypes.

This study shows WEE1 inhibitors work better with mRNA translation defects by activating GCN2, and suggests ways to reduce off-target effects.

This paper introduces RECODR, a computational pipeline that tracks transcriptome changes in cancer development and treatment to predict resistance mechanisms and design effective therapies.

This study shows that USP37 prevents premature TRAIP-mediated disassembly of stalled replisomes, maintaining genome stability under replication stress.

The paper introduces Exorcise, a tool to reannotate CRISPR libraries to user-defined genomes, improving targeting accuracy and reducing bias in screens.

This study identifies DCTD and TOPORS as key factors in decitabine cytotoxicity by showing their roles in DPC formation and repair.

This study identifies MDC1's role in replication fork restart and shows its loss leads to chemoresistance in BRCA1/2-deficient mammary tumors.

The paper uses a CRISPRi screen in human fetal lung organoids to identify SOX9 as a key regulator of progenitor self-renewal, showing it primes cells to receive WNT and RTK signals.

The paper investigates mutagenic mechanisms of cancer-associated DNA polymerase ε alleles, showing that exonuclease domain mutations cause ultra-mutagenesis with mutation patterns similar to cancer Signature 14.

The paper assesses how p53 status affects CRISPR-Cas9 screen performance by comparing wild-type and TP53 knockout cells, showing that optimal design can still yield reliable results.

The paper predicts Cas9-induced mutation outcomes based on surrounding DNA sequence using data from over 1 billion mutational outcomes.

This study shows that tau mutations in FTD cause hyperphosphorylation, mislocalization, and nuclear membrane deformation, leading to defective nucleocytoplasmic transport.

This paper describes a method to detect functional protein domains by identifying suppressor mutations in yeast and mouse cells, revealing insights into protein function and drug resistance mechanisms.