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Acknowledgements This work was supported by grants from the National Research Foundation of Korea (NRF-2015M3A9E6028674, NRF-2016R1A5A1010764, and NRF-2017M3A9D8064193), the Institute for Basic Science from the Ministry of Science, ICT, and Future Planning of Korea (IBS-R008-D1), and Suh Kyungbae Foundation

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Our results here support the model in which the cyclin D-Rb helix docking interaction drives Rb inactivation and cell-cycle progression in vivo