Lenalidomide: deciphering mechanisms of action in myeloma, myelodysplastic syndrome and beyond

被引：18
|
作者：
Guirguis, Andrew A. [1 ,2 ]
Ebert, Benjamin L. [1 ,2 ]
机构：
[1] Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 USA
[2] Broad Inst MIT & Harvard, Cambridge, MA 02142 USA
来源：
CURRENT OPINION IN CELL BIOLOGY | 2015年 / 37卷
关键词：
MULTIPLE-MYELOMA; PLUS DEXAMETHASONE; PROGNOSTIC IMPACT; TP53; MUTATIONS; CELL LYMPHOMA; OPEN-LABEL; LOW-RISK; THALIDOMIDE; IKAROS; CEREBLON;
D O I：
10.1016/j.ceb.2015.10.004
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Lenalidomide and its related 'analogues' modulate the substrate specificity of the CRL4CRBN E3 ubiquitin ligase complex. Polyubiquitination and subsequent proteasomal degradation of IKZF1 and IKZF3 in multiple myeloma and CK1 alpha in del(5q) MDS has recently been linked to therapeutic efficacy of this class of compounds. Harnessing ubiquitin ligase substrate specificity, may in time facilitate the degradation of other 'undruggable' proteins and allow for separation of detrimental side effects of IMiD compounds from those associated with therapeutic efficacy.
引用
收藏
页码：61 / 67
页数：7
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