NIH R01 · 2025
Molecular mechanisms of TAK1 regulation in rheumatoid arthritis
PROJECT SUMMARY In rheumatoid arthritis (RA), activated synovial fibroblasts (SFs) transform into an invasive phenotype that recruits immune cells to cause tissue destruction. Recent findings show transforming growth factor β-activated kinase 1 (TAK1) as a pivotal mediator of IL-1β, TNF-α, and Toll-like receptor signaling cascades due to its central position upstream of mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB) pathways. However, the molecular mechanism by which TAK1 regulates SF functions to promote RA pathogenesis remains unexplored. Using FAPα+Thy1+ RASFs, we showed that IL-1β-induced inflammatory signals are suppressed by inhibiting the TAK1 kinase domain…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.