YAP enters the mTOR pathway to promote tuberous sclerosis complex.
Mutations in tuberous sclerosis complex 1 (TSC1) or TSC2 predispose to angiomyolipomas and lymphangioleiomyomatosis in a mTOR-dependent manner. In these mesenchymal lesions, mTOR suppresses macroautophagy-mediated lysosomal degradation of YAP, which is a transcriptional coactivator of Hippo pathway and is required for the tumorigenesis of TSC. Therapeutic applications for TSC and other diseases with dysregulated mTOR activity can be envisaged.
Institut Necker-Enfants Malades; Paris, France; Inserm, U1151; Paris, France; Université Paris Descartes; Sorbonne Paris Cité; Paris, France.
Ning
N
Liang
Institut Necker-Enfants Malades; Paris, France; Inserm, U1151; Paris, France; Université Paris Descartes; Sorbonne Paris Cité; Paris, France.
Mario
M
Pende