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Journal article

53BP1 cooperation with the REV7–shieldin complex underpins DNA structure-specific NHEJ

Abstract:

53BP1 governs a specialized, context-specific branch of the classical non-homologous end joining DNA double-strand break repair pathway. Mice lacking 53bp1 (also known as Trp53bp1) are immunodeficient owing to a complete loss of immunoglobulin classswitch recombination1,2, and reduced fidelity of long-range V(D)J recombination3. The 53BP1-dependent pathway is also responsible for pathological joining events at dysfunctional telomeres4, and its unrestricted activity in Brca1-deficient cellular...

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Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/s41586-018-0362-1

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Institution:
University of Oxford
Division:
Medical Sciences
Department:
NDM; Human Genetics Wt Centre
Role:
Author
More by this author
Institution:
University of Oxford
Division:
Medical Sciences
Department:
NDM; Human Genetics Wt Centre
Role:
Author
More by this author
Institution:
University of Oxford
Division:
Medical Sciences
Department:
NDM; Human Genetics Wt Centre
Role:
Author
More by this author
Institution:
University of Oxford
Division:
Medical Sciences
Department:
NDM; Human Genetics Wt Centre
Role:
Author
More by this author
Institution:
University of Oxford
Division:
Medical Sciences
Department:
NDM; Human Genetics Wt Centre
Role:
Author
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More from this funder
Funding agency for:
Chapman, J
Grant:
C52690/A19270
John Fell Fund More from this funder
Kennedy Trust More from this funder
Publisher:
Springer Nature Publisher's website
Journal:
Nature Journal website
Volume:
560
Pages:
122–127
Publication date:
2018-07-25
Acceptance date:
2018-06-13
DOI:
ISSN:
1476-4687
Source identifiers:
870540
Pubs id:
pubs:870540
UUID:
uuid:8bf025bd-3564-45e6-97d2-4573cde7ed51
Local pid:
pubs:870540
Deposit date:
2018-07-16

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