Ordan J. Lehmann

The paper identifies FOXC1 as a transcription factor that enhances ARHGAP36 expression, increasing Hedgehog pathway activity and predicting improved neuroblastoma survival.

This paper shows that FOXC1 mutations in zebrafish cause left-right axis defects and congenital heart defects, similar to human Axenfeld-Rieger syndrome.

The paper shows that FOXC1 affects ciliation and cilia-dependent signaling, contributing to pleiotropic phenotypes in Axenfeld-Rieger Syndrome.

The paper traces the morphogenesis and transcriptome of early vascular smooth muscle cells in zebrafish using foxc1b as a marker.