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Q.LiuH.YangM.et al (2015)

Funding This work was supported by funding from the Sanming Project of Medicine in Shenzhen (SZSM201612051), the opening project of State Key Laboratory of Explosion Science and Technology (Beijing Institute of Technology, KFJJ22-16M), National Nature Science Foundation of China (81970467), and CAMS Innovation Fund for Medical Sciences (CIFMS, 2019-I2M-1-003)

247 Mutations in SMAD2/4 or their receptors, which are prone to ubiquitination, disrupt TGF- signaling and contribute to tumorigenesis