WIP Drives Tumor Progression through YAP/TAZ-Dependent Autonomous Cell Growth
文摘

High WIP levels promote YAP/TAZ stability and correlate with poor patient survival

WIP regulates the endocytic/endosomal system via Rac/PAK and the formin mDia

WIP expression leads to sequestration of the β-catenin destruction complex in MVB

WIP reduction impairs in vivo glioblastoma growth, notably increasing mouse survival

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