Summary
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 s
