USP22 regulates cell proliferation by deubiquitinating the transcriptional regulator FBP1

被引：132

作者：

Atanassov, Boyko S. ^{[1
,2
,3
]}

Dent, Sharon Y. R. ^{[1
,2
,3
]}

机构：

[1] Univ Texas MD Anderson Canc Ctr, Dept Mol Carcinogenesis, Smithville, TX 78957 USA

[2] Univ Texas MD Anderson Canc Ctr, Program Genes & Dev, Houston, TX 77030 USA

[3] Univ Texas MD Anderson Canc Ctr, Ctr Canc Epigenet, Houston, TX 77030 USA

来源：

EMBO REPORTS | 2011年 / 12卷 / 09期

关键词：

USP22; cell cycle; FBP1; p21; ubiquitin; ELEMENT-BINDING PROTEIN-1; C-MYC; HISTONE H2A; CANCER; OVEREXPRESSION; PROGRESSION; EXPRESSION; REPRESSION;

D O I：

10.1038/embor.2011.140

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Ubiquitin-specific protease 22 (USP22) edits the histone code by deubiquitinating H2A and H2B as part of the mammalian SAGA (Spt-Ada-Gcn5) complex, and is required for transcriptional regulation and normal cell-cycle progression. Here, we show that USP22 affects the expression of p21 by altering far upstream element (FUSE)-binding protein 1 (FBP1) ubiquitination, as ablation of USP22 leads to increased FBP1 ubiquitination and decreased FBP1 protein occupancy at the p21 gene. Surprisingly, increased polyubiquitination of FBP1 does not alter its protein stability, but instead modulates the stable recruitment of FBP1 to target loci. Our results indicate a mechanism by which USP22 regulates cell proliferation and tumorigenesis.

引用

页码：924 / 930

页数：7

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