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A new paper has been published.
A study performed in collaboration with Prof. Hiroshi Handa, Tokyo Medical University, and others has been
published in Nature Chemical Biology. In this study, we identified p63, a transcription factor of the p53 family, as a new substrate protein for the Cereblon (CRBN) E3 ubiquitin ligase, which is also known as a primary target of the drug thalidomide. Moreover, we demonstrated that ubiquitination and degradation of p63 by thalidomide/CRBN is underlying cause for thalidomide teratogenicity on the fetus. These findings are an important step toward the development of thalidomide-based medicines without teratogenicity. For more detail, please also take a look at
Tokyo Tech News.