Rebecca L. Ross

This study identifies AURKA/HDAC6 activation as a driver of primary cilia shortening and fibroblast activation in systemic sclerosis.

This study identifies ciliary program imbalance as a driver of fibroblast-to-myofibroblast reprogramming in systemic sclerosis, suggesting ciliotherapy as a potential treatment.

This paper identifies small molecules targeting the Tenascin C fibrinogen-like globe domain to reduce fibrosis in systemic sclerosis by inhibiting Toll-like receptor 4 signaling.

The paper shows that altering primary cilia length in fibroblasts can reduce fibrotic responses across different fibrotic conditions.

The paper identifies first-in-class inhibitors (BLUEs) that selectively inhibit BRISC complex activity by stabilizing an autoinhibited dimer, reducing interferon-stimulated gene expression.

This study shows CLIC4 regulates type 1 interferon signaling in SSc epithelial cells and inhibiting it blocks IFN pathway activation.