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JCAD promotes endothelial dysfunction and atherosclerosis. Junctional protein JCAD promotes the activation of YAP/TAZ/TEAD by interacting with TRIOBP and thus stabilizing F-actin stress fiber. By doing so, JCAD trigger the expression of inflammatory genes in endothelial cells, driving an inflammatory process via the recruitment of monocytes and resulting in the formation of atherosclerotic plaques.
