Evidence map›Paper›PMID 27550810›Full record

ArticleMolecular and cellular biology2016

DEAD Box 1 Facilitates Removal of RNA and Homologous Recombination at DNA Double-Strand Breaks.

Lei Li, Devon R Germain, Ho-Yin Poon, Matthew R Hildebrandt, Elizabeth A Monckton, Darin McDonald, Michael J Hendzel, Roseline Godbout

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

99 citing papers in PubMed, 152 citations in OpenAlex.

  1. Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026
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  4. Enzymology of the metazoan tRNA ligase complex: a lifetime in cycles.Cellular and molecular life sciences : CMLS · 2026
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  20. Review

39 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

8 authors at 1 institution in 1 country.

Lei LiDepartment of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, Alberta, Canada.
Devon R GermainDepartment of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, Alberta, Canada.
Ho-Yin PoonDepartment of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, Alberta, Canada.
Matthew R HildebrandtDepartment of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, Alberta, Canada.
Elizabeth A MoncktonDepartment of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, Alberta, Canada.
Darin McDonaldDepartment of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, Alberta, Canada.
Michael J HendzelDepartment of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, Alberta, Canada.
Roseline GodboutDepartment of Oncology, University of Alberta, Cross Cancer Institute, Edmonton, Alberta, Canada rgodbout@ualberta.ca.
University of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although RNA and RNA-binding proteins have been linked to double-strand breaks (DSBs), little is known regarding their roles in the cellular response to DSBs and, if any, in the repair process. Here, we provide direct evidence for the presence of RNA-DNA hybrids at DSBs and suggest that binding of RNA to DNA at DSBs may impact repair efficiency. Our data indicate that the RNA-unwinding protein DEAD box 1 (DDX1) is required for efficient DSB repair and cell survival after ionizing radiation (IR), with depletion of DDX1 resulting in reduced DSB repair by homologous recombination (HR). While DDX1 is not essential for end resection, a key step in homology-directed DSB repair, DDX1 is required for maintenance of the single-stranded DNA once generated by end resection. We show that transcription deregulation has a significant effect on DSB repair by HR in DDX1-depleted cells and that RNA-DNA duplexes are elevated at DSBs in DDX1-depleted cells. Based on our combined data, we propose a role for DDX1 in resolving RNA-DNA structures that accumulate at DSBs located at sites of active transcription. Our findings point to a previously uncharacterized requirement for clearing RNA at DSBs for efficient repair by HR.

Indexed as

DNA RepairHomologous RecombinationCell LineCell SurvivalDEAD-box RNA HelicasesDNA Breaks, Double-StrandedGene Expression RegulationHeLa CellsHumansRNATranscription, GeneticDDX1 protein, humanDEAD-box RNA HelicasesRNA

Identifiers

PMID27550810
PMCPMC5086521
OpenAlexW2517720692

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.