Evidence map›Paper›PMID 26880199›Full record

ArticleThe Journal of cell biology2016

MRN, CtIP, and BRCA1 mediate repair of topoisomerase II-DNA adducts.

Tomas Aparicio, Richard Baer, Max Gottesman, Jean Gautier

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
10.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

90 citing papers in PubMed, 128 citations in OpenAlex.

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  17. Editorial: The repair of DNA-protein crosslinks.Frontiers in molecular biosciences · 2023
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30 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Tomas AparicioInstitute for Cancer Genetics, Columbia University, New York, NY, 10032.
Richard BaerInstitute for Cancer Genetics, Columbia University, New York, NY, 10032.
Max GottesmanDepartment of Biochemistry and Biophysics, Columbia University, New York, NY, 10032.
Jean GautierInstitute for Cancer Genetics, Columbia University, New York, NY, 10032 Department of Genetics and Development, Columbia University, New York, NY, 10032 jg130@columbia.edu.
Cancer Genetics (United States) · USColumbia University · US

Funding

The Role of CTIP in Lymphocyte Development and LymphomagenesisP01CA174653 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI RABADAN, RAUL · 2014 to 2024
$17.6M
DNA Repair and Genomic Instability in Cancer Development and TherapyR35CA197606 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GAUTIER, JEAN · 2015 to 2021
$5.7M
Regulation of the DNA damage response by the MRN-ATM pathwayR01CA092245 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GAUTIER, JEAN · 2002 to 2015
$4.0M
Studies of DNA interstrand crosslink repair to improve crosslinking drug therapieR01CA167826 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GAUTIER, JEAN · 2012 to 2015
$1.3M
NCI NIH HHS CA092245NCI NIH HHS CA167826NCI NIH HHS CA174653NCI NIH HHS P01 CA174653NCI NIH HHS R01 CA092245NCI NIH HHS R01 CA167826NCI NIH HHS R35 CA197606
6 · The paper itself

Abstract

Repair of DNA double-strand breaks (DSBs) with complex ends poses a special challenge, as additional processing is required before DNA ligation. For example, protein-DNA adducts must be removed to allow repair by either nonhomologous end joining or homology-directed repair. Here, we investigated the processing of topoisomerase II (Top2)-DNA adducts induced by treatment with the chemotherapeutic agent etoposide. Through biochemical analysis in Xenopus laevis egg extracts, we establish that the MRN (Mre11, Rad50, and Nbs1) complex, CtIP, and BRCA1 are required for both the removal of Top2-DNA adducts and the subsequent resection of Top2-adducted DSB ends. Moreover, the interaction between CtIP and BRCA1, although dispensable for resection of endonuclease-generated DSB ends, is required for resection of Top2-adducted DSBs, as well as for cellular resistance to etoposide during genomic DNA replication.

Indexed as

DNA Breaks, Double-StrandedDNA RepairAnimalsAntigens, NeoplasmBRCA1 ProteinCarrier ProteinsDNA AdductsDNA-Binding ProteinsDNA Repair EnzymesDNA ReplicationDNA Topoisomerases, Type IIEtoposideFemaleMRE11 Homologue ProteinMultiprotein ComplexesTime FactorsAntigens, NeoplasmBRCA1 ProteinCarrier ProteinsDNA AdductsDNA-Binding ProteinsDNA Repair EnzymesDNA Topoisomerases, Type IIEtoposideMRE11 Homologue ProteinMre11 protein, XenopusMultiprotein ComplexesNBN protein, XenopusRad50 protein, XenopusRBBP8 protein, XenopusTopoisomerase II InhibitorsTumor Suppressor ProteinsXenopus Proteins

Identifiers

PMID26880199
PMCPMC4754713
OpenAlexW2275231116

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.