J. Karapurkar

LATS1/2 inactivation drives a distinct venous endothelial cell response that contributes to fibrotic remodeling of the lung

Endothelial dysfunction is recognized to contribute to chronic tissue remodeling in the lung, yet endothelial-derived mechanisms driving these processes remain largely undefined. Here, we show that endothelial inactivation of the LATS1 and LATS2 kinases, key suppressors of the transcriptional regulators YAP and TAZ, el...