Evidence map›Paper›PMID 24005565›Full record

ArticleNature communications2013

Human DNA helicase HELQ participates in DNA interstrand crosslink tolerance with ATR and RAD51 paralogs.

Kei-ichi Takata, Shelley Reh, Junya Tomida, Maria D Person, Richard D Wood

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

52 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Helicase HELQ: Molecular Characters Fit for DSB Repair Function.International journal of molecular sciences · 2024
    Review
  8. Article
  9. A Human HomozygousGenes · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Genes · 2022
    Article
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

5 authors at 2 institutions in 1 country.

Kei-ichi TakataDepartment of Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center Science Park, Smithville, TX 78957, USA.
Shelley Reh
Junya Tomida
Maria D Person
Richard D Wood
The University of Texas MD Anderson Cancer Center · USThe University of Texas at Austin · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Pilot Project ProgramP30ES007784 · NIEHS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI RICHIE, ELLEN R · 1996 to 2011
$16.4M
Recognition and processing of complex lesions by components from multiple DNAP01CA097175 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI NAIRN, RODNEY S · 2004 to 2014
$15.3M
NCI NIH HHS P01 CA09717NCI NIH HHS P01 CA097175NCI NIH HHS P30 CA016672NCI NIH HHS P30-CA016672NIEHS NIH HHS P30 ES007784
6 · The paper itself

Abstract

Mammalian HELQ is a 3'-5' DNA helicase with strand displacement activity. Here we show that HELQ participates in a pathway of resistance to DNA interstrand crosslinks (ICLs). Genetic disruption of HELQ in human cells enhances cellular sensitivity and chromosome radial formation by the ICL-inducing agent mitomycin C (MMC). A significant fraction of MMC sensitivity is independent of the Fanconi anaemia pathway. Sister chromatid exchange frequency and sensitivity to UV radiation or topoisomerase inhibitors is unaltered. Proteomic analysis reveals that HELQ is associated with the RAD51 paralogs RAD51B/C/D and XRCC2, and with the DNA damage-responsive kinase ATR. After treatment with MMC, reduced phosphorylation of the ATR substrate CHK1 occurs in HELQ-knockout cells, and accumulation of G2/M cells is reduced. The results indicate that HELQ operates in an arm of DNA repair and signalling in response to ICL. Further, the association with RAD51 paralogs suggests HELQ as a candidate ovarian cancer gene.

Indexed as

Sequence Homology, Amino AcidAtaxia Telangiectasia Mutated ProteinsBase SequenceCell LineCheckpoint Kinase 1Cross-Linking ReagentsDNADNA Copy Number VariationsDNA DamageDNA HelicasesEnzyme ActivationFanconi AnemiaFanconi Anemia Complementation Group D2 ProteinFemaleGene Knockout TechniquesHEK293 CellsAtaxia Telangiectasia Mutated ProteinsATR protein, humanCheckpoint Kinase 1CHEK1 protein, humanCross-Linking ReagentsDNADNA HelicasesFANCD2 protein, humanFanconi Anemia Complementation Group D2 ProteinHELQ protein, humanMitomycinMutant ProteinsProtein KinasesRAD51 protein, humanRad51 Recombinase

Identifiers

PMID24005565
PMCPMC3778836
OpenAlexW2026877007

What OpenQuestion holds

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LicenceCC BY
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.