Licensed to elongate: a molecular mechanism for MLL-based leukaemogenesis

被引：141

作者：

Mohan, Man ^{[1
]}

Lin, Chengqi ^{[1
]}

Guest, Erin ^{[1
,2
]}

Shilatifard, Ali ^{[1
]}

机构：

[1] Stowers Inst Med Res, Kansas City, MO 64110 USA

[2] Childrens Mercy Hosp, Kansas City, MO 64108 USA

来源：

NATURE REVIEWS CANCER | 2010年 / 10卷 / 10期

关键词：

RNA-POLYMERASE-II; ACUTE MYELOID-LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; PROTO-ONCOPROTEIN MLL; HISTONE METHYLTRANSFERASE COMPLEX; TRANSCRIPTIONAL ELONGATION; GENE-EXPRESSION; H3K4; METHYLATION; CHROMATIN MODIFICATION; DROSOPHILA-TRITHORAX;

D O I：

10.1038/nrc2915

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The RNA polymerase II (Pol II) elongation factor (ELL) was the first translocation partner of mixed lineage leukaemia (MLL) for which a biochemical function was determined. It was therefore proposed that the regulation of the elongation stage of transcription could be fundamental to MLL-based leukaemogenesis. Recent studies have identified ELL complexed with several of the translocation partners of MLL in a transcriptional super elongation complex (SEC). These studies provide evidence for the importance of the regulation of Pol II elongation in disease pathogenesis and suggest that MLL chimaeras function by licensing Pol II transcription elongation without the appropriate checkpoints.

引用

收藏

页码：720 / 728

页数：9

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