Elimination of mutant SWI/SNF complexes by protein quality control: new opportunities targeting aggressive rhabdoid tumours  

作　　者：Andreas Krämer Stefan Knapp 

机构地区：[1]Institute of Pharmaceutical Chemistry,Goethe University Frankfurt,Max-von-Laue-Str.9,60438,Frankfurt am Main,Germany [2]Structural Genomics Consortium,Buchmann Institute for Molecular Life Sciences,Goethe-University Frankfurt,Max-von-Laue-Str.15,60438,Frankfurt am Main,Germany [3]German Cancer Consortium(DKTK),German Cancer Research Center(DKFZ),DTKT Site Frankfurt-Mainz,69120,Heidelberg,Germany

出　　处：《Signal Transduction and Targeted Therapy》2024年第10期4151-4153,共3页信号转导与靶向治疗（英文）

基　　金：German translational cancer network(DKTK),the Frankfurt Cancer Institute(FCI);German Cancer Aid(Krebshilfe)grant TACTIC and the SFB1430(Molecular Mechanisms of Cell State Transitions)。

摘　　要：A recent study published in Nature by Radko-Juettner and colleagues reports an unexpected mutant-specific synthetic lethality in which the E3 protein ubiquitin ligase DCAF5 specifically degrades mutant but not wild-type SWI/SNF chromatin remodeling complexes.1 DCAF5 contains a likely druggable WDR domain,providing a new avenue for the development of novel therapeutics for aggressive cancers with SMARCB1 loss of function mutations.

关 键 词：TUMOUR LIKELY COMPLEXES 

分 类 号：R44[医药卫生—诊断学]