Loss of Mob1a/b in mice results in chondrodysplasia due to YAP1/TAZ-TEAD-dependent repression of SOX9 - Goto, Hiroki; Nishio, Miki; To, Yoko; Oishi, Tatsuya; Miyachi, Yosuke; Maehama, Tomohiko; Nishina, Hiroshi; Akiyama, Haruhiko; Mak, Tak Wah; Makii, Yuma; Saito, Taku; Yasoda, Akihiro; et al. (Development (Cambridge), 2018)
Keywords: Adaptor proteins; Adaptor Proteins, Signal Transducing - metabolism; Animals; Blotting, Western; Cartilage; Cell Culture Techniques; Cell Cycle Proteins; Cell density; Cell Differentiation - genetics; Cell Proliferation - genetics; Chondrocytes; Chondrocytes - metabolism; Chondrodystrophy; Chondrogenesis; Chondrogenesis - genetics; Chromatin Immunoprecipitation; Clonal deletion; Endochondral bone; Extracellular matrix; Gene Expression Regulation; Growth factors; Immunohistochemistry; Intracellular Signaling Peptides and Proteins; Kinases; Mice; Molecular modelling; Ossification; Osteochondrodysplasias - genetics; Osteochondrodysplasias - metabolism; Phosphoproteins - metabolism; Real-Time Polymerase Chain Reaction; Rodents; Signal Transduction; Sox9 protein; SOX9 Transcription Factor - metabolism; Tamoxifen; Trans-Activators; Transcription factors; Yes-associated protein; YAP1; WWTR1; Mouse; MOB1; Chondrocytes; Chondrodysplasia; SOX9; TAZ