Structural basis of lenalidomide-induced CK1α degradation by the CRL4CRBN ubiquitin ligase

Georg Petzold, Eric S. Fischer and Nicolas H. Thomä ()
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Georg Petzold: Friedrich Miescher Institute for Biomedical Research
Eric S. Fischer: Friedrich Miescher Institute for Biomedical Research
Nicolas H. Thomä: Friedrich Miescher Institute for Biomedical Research

Nature, 2016, vol. 532, issue 7597, 127-130

Abstract: Thalidomide and its derivative lenalidomide bind the CRL4CRBN E3 ubiquitin ligase and target protein substrates for degradation; structural and functional data determined here show that casein kinase 1α and the lymphoid transcription factor Ikaros, the efficacy targets of lenalidomide in two different blood cancers, interact with the CRBN–lenalidomide interface through a β-hairpin destruction motif.

Date: 2016
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DOI: 10.1038/nature16979

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