R. A. Grant

The paper shows that prolonged exposure to lung-derived cytokines in COVID-19 patients activates microglia, and corticosteroids reduce this inflammatory response.

The paper investigates how the Pro283 substitution in influenza nucleoprotein affects protein folding and aggregation, revealing it increases aggregation propensity without altering native structure.

The paper identifies profibrotic monocyte-derived alveolar macrophages and neutrophil recruitment as drivers of lung fibrosis in patients with persistent respiratory symptoms and radiographic abnormalities after COVID-19.

The paper identifies new BAK binders that show similar binding modes and kinetics to both activators and inhibitors, suggesting sequence-function relationships are not determined by affinity or kinetics.

The paper identifies a conformational mechanism enabling specificity in ENAH EVH1 binding to PCARE, and designs a highly selective inhibitor.

The paper identifies how proline-rich motifs interact with ENAH EVH1 domain through sequence context, revealing extended SLiMs and their role in protein-protein interactions.

The paper identifies a positive feedback loop between SARS-CoV-2-infected alveolar macrophages and T cells in severe COVID-19 patients, driving persistent alveolitis.

ISRIB reduces pulmonary fibrosis severity in young and old mice by modulating stress response signaling in alveolar epithelial cells.

This study examines proteome changes in alveolar macrophages and type 2 cells from young and old mice before and after influenza infection, revealing age-related proteostasis and mitochondrial dysfunction that worsen with infection.