James M. Burke

This study shows adenovirus mutants differentially activate dsRNA sensors, leading to distinct RNP granule assemblies via PKR and OAS3/RNase L pathways.

This study compares how SARS-CoV-2 and MERS-CoV nsp1 proteins affect host protein synthesis and the integrated stress response, revealing differential impacts on eIF2 phosphorylation and stress granule formation.

This study evaluates whether deubiquitylases (DUBs) can be effectively degraded by PROTACs, finding that some DUBs are degradable while others resist degradation due to auto-deubiquitylation or poor proteasome substrate properties.

This study shows that adding an imidazopyridinium (IP+) unit to macrocyclic peptides enhances their passive membrane permeability, enabling them to enter cells and inhibit intracellular targets like p53-MDM2.

The paper identifies RNA binding by mutant p53 and shows it contributes to mitochondrial dysfunction through altered miRNA processing.

This study shows MERS-CoV inhibits PKR activation by blocking its condensation on viral dsRNA, revealing a mechanism by which the virus evades innate immune responses.

The paper develops STAR-FACS to sort cells by SNVs and shows distinct transcriptomes in glioblastoma cells with different TERT promoter mutations.

This study shows RNase L reduces antiviral proteins by inhibiting mRNA export and RNAPII-mediated transcription during flavivirus infection.

The paper shows that RNase L-induced bodies sequester subgenomic flavivirus RNAs, reducing their interaction with P-bodies and enhancing viral RNA decay.

This study shows that SARS-CoV-2 nsp15 inhibits dsRNA-induced antiviral signaling, which is necessary for viral replication in nasal epithelial cultures.

The paper develops a compact shRNA expression system using retroviral miRNA gene architecture, reducing coding space needed for shRNA expression by over two-fold compared to U6/H1 promoters.