Evidence map›Paper›PMID 30244837›Full record

ArticleMolecular cell2018

The BRCT Domains of the BRCA1 and BARD1 Tumor Suppressors Differentially Regulate Homology-Directed Repair and Stalled Fork Protection.

David Billing, Michiko Horiguchi, Foon Wu-Baer, Angelo Taglialatela, Giuseppe Leuzzi, Silvia Alvarez Nanez, Wenxia Jiang, Shan Zha, Matthias Szabolcs, Chyuan-Sheng Lin and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 82 citations in OpenAlex.

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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

12 authors at 3 institutions in 1 country.

David BillingInstitute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY 10032, USA; Department of Pathology & Cell Biology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Michiko HoriguchiInstitute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY 10032, USA; Department of Pathology & Cell Biology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Foon Wu-BaerInstitute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY 10032, USA; Department of Pathology & Cell Biology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Angelo TaglialatelaDepartment of Genetics & Development, Columbia University Irving Medical Center, New York, NY 10032, USA.
Giuseppe LeuzziDepartment of Genetics & Development, Columbia University Irving Medical Center, New York, NY 10032, USA.
Silvia Alvarez NanezDepartment of Genetics & Development, Columbia University Irving Medical Center, New York, NY 10032, USA.
Wenxia JiangInstitute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY 10032, USA; Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, NY 10032, USA.
Shan ZhaInstitute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY 10032, USA; Department of Pathology & Cell Biology, Columbia University Irving Medical Center, New York, NY 10032, USA; Department of Pediatrics, Columbia University Irving Medical Center, New York, NY 10032, USA; Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, NY 10032, USA.
Matthias SzabolcsDepartment of Pathology & Cell Biology, Columbia University Irving Medical Center, New York, NY 10032, USA; Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, NY 10032, USA.
Chyuan-Sheng LinDepartment of Pathology & Cell Biology, Columbia University Irving Medical Center, New York, NY 10032, USA; Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, NY 10032, USA.
Alberto CicciaDepartment of Genetics & Development, Columbia University Irving Medical Center, New York, NY 10032, USA; Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, NY 10032, USA.
Richard BaerInstitute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY 10032, USA; Department of Pathology & Cell Biology, Columbia University Irving Medical Center, New York, NY 10032, USA; Herbert Irving Comprehensive Cancer Center, Columbia University Irving Medical Center, New York, NY 10032, USA. Electronic address: rb670@columbia.edu.
Columbia University Irving Medical Center · USCancer Genetics (United States) · USColumbia University · US

Funding

Tumor Biology and Microenvironment ProgramP30CA013696 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Parisa Tehranifar · 1985 to 2026
$115.3M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM007367 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI REINER, STEVEN L · 1985 to 2021
$25.1M
The Role of CTIP in Lymphocyte Development and LymphomagenesisP01CA174653 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SYMINGTON, LORRAINE S · 2014 to 2024
$17.6M
Replication fork remodeling and genomic stabilityR01CA197774 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Alberto Ciccia · 2016 to 2026
$4.2M
The BARD1 tumor suppressor and breast cancerR01CA172272 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BAER, RICHARD J · 2013 to 2017
$1.7M
The role of the BARD1 BRCT domains in DNA repair and tumor suppressionF31CA200181 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BILLING, DAVID LEE · 2015 to 2016
$89k
NCI NIH HHS F31 CA200181NCI NIH HHS P01 CA174653NCI NIH HHS P30 CA013696NCI NIH HHS R01 CA172272NCI NIH HHS R01 CA197774NIGMS NIH HHS T32 GM007367
6 · The paper itself

Abstract

The BRCA1 tumor suppressor preserves genome integrity through both homology-directed repair (HDR) and stalled fork protection (SFP). In vivo, BRCA1 exists as a heterodimer with the BARD1 tumor suppressor, and both proteins harbor a phosphate-binding BRCT domain. Here, we compare mice with mutations that ablate BRCT phospho-recognition by Bard1 (Bard1

Indexed as

AnimalsBRCA1 ProteinChromosomal InstabilityDNA Breaks, Double-StrandedDNA RepairFemaleHumansMiceMutationProtein DomainsRecombinational DNA RepairTumor Suppressor ProteinsUbiquitin-Protein LigasesBard1 protein, mouseBRCA1 ProteinBrca1 protein, mouseTumor Suppressor ProteinsUbiquitin-Protein LigasesBARD1BRCA1BRCT domainDNA break repairfamilial breast cancergenome instabilitypoly(ADP-ribose)stalled replication forkstumor suppression

Identifiers

PMID30244837
PMCPMC6347115
OpenAlexW2890415599

What OpenQuestion holds

Textmetadata
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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.