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The ASCIZ-DYNLL1 axis promotes 53BP1-dependent non-homologous end joining and PARP inhibitor sensitivity

Abstract:

53BP1 controls a specialized non-homologous end joining (NHEJ) pathway that is essential for adaptive immunity, yet oncogenic in BRCA1 mutant cancers. Intra-chromosomal DNA double-strand break (DSB) joining events during immunoglobulin class switch recombination (CSR) require 53BP1. However, in BRCA1 mutant cells, 53BP1 blocks homologous recombination (HR) and promotes toxic NHEJ, resulting in genomic instability. Here, we identify the protein dimerization hub—DYNLL1—as an organizer of multim...

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Publication status:
Published
Peer review status:
Peer reviewed
Version:
Publisher's version

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Publisher copy:
10.1038/s41467-018-07855-x

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Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
NDM
Subgroup:
Human Genetics Wt Centre
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Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
NDM
Subgroup:
Human Genetics Wt Centre
Barazas, M More by this author
More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
NDM
Subgroup:
Human Genetics Wt Centre
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Funding agency for:
Cuella-Martin, R
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Funding agency for:
Blackford, AN
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Funding agency for:
Chapman, JR
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Grant:
Wellcome core award 090532/Z/09/Z
Publisher:
Springer Nature Publisher's website
Journal:
Nature Communications Journal website
Volume:
9
Pages:
Article: 5406
Publication date:
2018-12-17
Acceptance date:
2018-11-30
DOI:
ISSN:
2041-1723
Pubs id:
pubs:949268
URN:
uri:3f8903b5-e0c0-4bfe-9bf0-35bcdd2479c6
UUID:
uuid:3f8903b5-e0c0-4bfe-9bf0-35bcdd2479c6
Local pid:
pubs:949268

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