53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress

被引：0

作者：

Claudia Lukas

Velibor Savic

Simon Bekker-Jensen

Carsten Doil

Beate Neumann

Ronni Sølvhøj Pedersen

Merete Grøfte

Kok Lung Chan

Ian David Hickson

Jiri Bartek

Jiri Lukas

机构：

[1] Centre for Genotoxic Stress Research,Department of Biochemistry

[2] Institute of Cancer Biology,Department of Cellular and Molecular Medicine

[3] Danish Cancer Society,undefined

[4] The Novo Nordisk Foundation Center for Protein Research,undefined

[5] University of Copenhagen,undefined

[6] Advanced Light Microscopy Facility,undefined

[7] European Molecular Biology Laboratory (EMBL),undefined

[8] Weatherall Institute of Molecular Medicine,undefined

[9] University of Oxford,undefined

[10] University of Oxford,undefined

[11] Center for Healthy Aging,undefined

[12] University of Copenhagen,undefined

[13] Institute of Molecular and Translational Medicine,undefined

[14] Palacky University,undefined

[15] 775 15,undefined

来源：

Nature Cell Biology | 2011年 / 13卷

关键词：

D O I：

暂无

中图分类号：

学科分类号：

摘要：

53BP1 is marker of double-strand breaks and accumulates in nuclear foci. These foci are shown to accumulate in G1 at lesions generated by replication stress and may shield lesions from erosion.

引用

页码：243 / 253

页数：10

共 43 条

[41] H3K9me3 and H4K20me3 represent the epigenetic landscape for 53BP1 binding to DNA lesions
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[43] Rad53-Mediated Regulation of Rrm3 and Pif1 DNA Helicases Contributes to Prevention of Aberrant Fork Transitions under Replication Stress
Rossi, Silvia Emma
Ajazi, Arta
Carotenuto, Walter
Foiani, Marco
Giannattasio, Michele
CELL REPORTS, 2015, 13 (01): : 80 - 92

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