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

[1] 53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress
Lukas, Claudia
Savic, Velibor
Bekker-Jensen, Simon
Doil, Carsten
Neumann, Beate
Pedersen, Ronni Solvhoj
Grofte, Merete
Chan, Kok Lung
Hickson, Ian David
Bartek, Jiri
Lukas, Jiri
NATURE CELL BIOLOGY, 2011, 13 (03) : 243 - U380
[2] Around and beyond 53BP1 Nuclear Bodies
Fernandez-Vidal, Anne
Vignard, Julien
Mirey, Gladys
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2017, 18 (12)
[3] 53BP1 nuclear bodies enforce replication timing at under-replicated DNA to limit heritable DNA damage
Spies, Julian
Lukas, Claudia
Somyajit, Kumar
Rask, Maj-Britt
Lukas, Jiri
Neelsen, Kai John
NATURE CELL BIOLOGY, 2019, 21 (04) : 487 - +
[4] 53BP1 nuclear bodies enforce replication timing at under-replicated DNA to limit heritable DNA damage
Julian Spies
Claudia Lukas
Kumar Somyajit
Maj-Britt Rask
Jiri Lukas
Kai John Neelsen
Nature Cell Biology, 2019, 21 : 487 - 497
[5] Mitotic regulators TPX2 and Aurora A protect DNA forks during replication stress by counteracting 53BP1 function
Byrum, Andrea K.
Carvajal-Maldonado, Denisse
Mudge, Miranda C.
Valle-Garcia, David
Majid, Mona C.
Patel, Romil
Sowa, Mathew E.
Gygi, Steven P.
Harper, J. Wade
Shi, Yang
Vindigni, Alessandro
Mosammaparast, Nima
JOURNAL OF CELL BIOLOGY, 2019, 218 (02): : 422 - 432
[6] 53BP1 Mediates ATR-Chk1 Signaling and Protects Replication Forks under Conditions of Replication Stress
Her, Joonyoung
Ray, Chandni
Altshuler, Jake
Zheng, Haiyan
Bunting, Samuel F.
MOLECULAR AND CELLULAR BIOLOGY, 2018, 38 (08)
[7] The RIF1-long splice variant promotes G1 phase 53BP1 nuclear bodies to protect against replication stress
Watts, Lotte P.
Natsume, Toyoaki
Saito, Yuichiro
Garzon, Javier
Dong, Qianqian
Boteva, Lora
Gilbert, Nick
Kanemaki, Masato T.
Hiraga, Shin-ichiro
Donaldson, Anne D.
ELIFE, 2020, 9 : 1 - 26
[8] The demise of a TUDOR under stress opens a chromatin link to 53BP1
Stewart, Grant S.
EMBO JOURNAL, 2012, 31 (08): : 1847 - 1849
[9] Phosphorylation and rapid relocalization of 53BP1 to nuclear foci upon DNA damage
Anderson, L
Henderson, C
Adachi, Y
MOLECULAR AND CELLULAR BIOLOGY, 2001, 21 (05) : 1719 - 1729
[10] ATMIN is required for the ATM-mediated signaling and recruitment of 53BP1 to DNA damage sites upon replication stress
Schmidt, Luisa
Wiedner, Marc
Velimezi, Georgia
Prochazkova, Jana
Owusu, Michel
Bauer, Sabine
Loizou, Joanna I.
DNA REPAIR, 2014, 24 : 122 - 130

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