Regulation of cell differentiation by the DNA damage response

被引：81

作者：

Sherman, Mara H. ^{[2
]}

Bassing, Craig H. ^{[1
,3
]}

Teitell, Michael A. ^{[2
,4
,5
]}

机构：

[1] Childrens Hosp Philadelphia, Ctr Childhood Canc Res, Dept Pathol & Lab Med, Div Canc Pathobiol, Philadelphia, PA 19104 USA

[2] Univ Calif Los Angeles, Inst Mol Biol, Los Angeles, CA 90095 USA

[3] Univ Penn, Sch Med, Abramson Family Canc Res Inst, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA

[4] Univ Calif Los Angeles, Calif NanoSyst Inst, Broad Stem Cell Res Ctr,Dept Pediat, Jonsson Comprehens Canc Ctr,Dept Pathol & Lab Med, Los Angeles, CA 90095 USA

[5] Univ Calif Los Angeles, Bioengn Interdept Program, Los Angeles, CA 90095 USA

来源：

TRENDS IN CELL BIOLOGY | 2011年 / 21卷 / 05期

基金：

美国国家卫生研究院;

关键词：

HEMATOPOIETIC STEM-CELLS; GERMINAL CENTER; SELF-RENEWAL; P53; ATM; STRESS; MAINTENANCE; EXPRESSION; CANCER; REPAIR;

D O I：

10.1016/j.tcb.2011.01.004

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

When faced with DNA double-strand breaks (DSBs), vertebrate cells activate DNA damage response (DDR) programs that preserve genome integrity and suppress malignant transformation. Three established outcomes of the DDR include transient cell cycle arrest coupled with DNA repair, apoptosis, or senescence. However, recent studies in normal and cancer precursor or stem cells suggest that a fourth potential outcome, cell differentiation, is under the influence of DDR programs. Here we review and discuss the emerging evidence that supports the linkage of signaling from DSBs to the regulation of differentiation, including some of the molecular mechanisms driving this under-appreciated DDR outcome. We also consider the physiologic and pathologic consequences of defects in DDR signaling on cell differentiation and malignant transformation.

引用

页码：312 / 319

页数：8

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