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

被引：0

作者：

Georg Petzold

Eric S. Fischer

Nicolas H. Thomä

机构：

[1] Friedrich Miescher Institute for Biomedical Research,

[2] University of Basel,undefined

[3] †Present addresses: Department of Cancer Biology,undefined

[4] Dana-Farber Cancer Institute,undefined

[5] LC-4312,undefined

[6] 360 Longwood Avenue,undefined

[7] Boston,undefined

[8] Massachusetts 02215,undefined

[9] USA; Department of Biological Chemistry and Molecular Pharmacology,undefined

[10] Harvard Medical School,undefined

[11] Boston,undefined

[12] Massachusetts 02215,undefined

[13] USA.,undefined

来源：

Nature | 2016年 / 532卷

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D O I：

暂无

中图分类号：

学科分类号：

摘要：

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.

引用

页码：127 / 130

页数：3

共 36 条

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