Evidence map›Paper›PMID 26920759›Full record

ArticleGenetics2016

MTE1 Functions with MPH1 in Double-Strand Break Repair.

Askar Yimit, TaeHyung Kim, Ranjith P Anand, Sarah Meister, Jiongwen Ou, James E Haber, Zhaolei Zhang, Grant W Brown

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 16 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

8 authors at 2 institutions in 2 countries.

Askar YimitDepartment of Biochemistry, University of Toronto, Toronto, Ontario M5S 3E1, Canada Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada.
TaeHyung KimDonnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada Department of Computer Science, University of Toronto, Toronto, Ontario M5S 3E1, Canada.
Ranjith P AnandRosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02453.
Sarah MeisterDepartment of Biochemistry, University of Toronto, Toronto, Ontario M5S 3E1, Canada Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada.
Jiongwen OuDepartment of Biochemistry, University of Toronto, Toronto, Ontario M5S 3E1, Canada Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada.
James E HaberRosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02453.
Zhaolei ZhangDonnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada Department of Computer Science, University of Toronto, Toronto, Ontario M5S 3E1, Canada.
Grant W BrownDepartment of Biochemistry, University of Toronto, Toronto, Ontario M5S 3E1, Canada Donnelly Centre, University of Toronto, Toronto, Ontario M5S 3E1, Canada grant.brown@utoronto.ca.ORCID 0000-0002-9002-5003
University of Toronto · CABrandeis University · US

Funding

Recombination Mechanisms in Yeast Cell DifferentiationR37GM020056 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2007 to 2016
$5.5M
Analysis of Break-Induced ReplicationR01GM076020 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2006 to 2017
$3.4M
NIGMS NIH HHS R01 GM076020NIGMS NIH HHS R37 GM020056
6 · The paper itself

Abstract

Double-strand DNA breaks occur upon exposure of cells to ionizing radiation and certain chemical agents or indirectly through replication fork collapse at DNA damage sites. If left unrepaired, double-strand breaks can cause genome instability and cell death, and their repair can result in loss of heterozygosity. In response to DNA damage, proteins involved in double-strand break repair by homologous recombination relocalize into discrete nuclear foci. We identified 29 proteins that colocalize with recombination repair protein Rad52 in response to DNA damage. Of particular interest, Ygr042w/Mte1, a protein of unknown function, showed robust colocalization with Rad52. Mte1 foci fail to form when the DNA helicase gene MPH1 is absent. Mte1 and Mph1 form a complex and are recruited to double-strand breaks in vivo in a mutually dependent manner. MTE1 is important for resolution of Rad52 foci during double-strand break repair and for suppressing break-induced replication. Together our data indicate that Mte1 functions with Mph1 in double-strand break repair.

Indexed as

DNA Breaks, Double-StrandedDNA RepairDEAD-box RNA HelicasesDNA-Binding ProteinsDNA DamageDNA ReplicationHomologous RecombinationProtein BindingProtein TransportRad52 DNA Repair and Recombination ProteinTelomere-Binding ProteinsDEAD-box RNA HelicasesDNA-Binding ProteinsRad52 DNA Repair and Recombination ProteinTelomere-Binding Proteinsbreak-induced replicationDNA repairdouble-strand breaksloss of heterozygositynuclear focirecombination

Identifiers

PMID26920759
PMCPMC4858770
OpenAlexW2335499581

What OpenQuestion holds

Textmetadata
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.