Evidence map›Paper›PMID 10629056›Full record

ArticleMolecular and cellular biology2000

Triple-helix formation induces recombination in mammalian cells via a nucleotide excision repair-dependent pathway.

A F Faruqi, H J Datta, D Carroll, M M Seidman, P M Glazer

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. 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
4.2field-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

52 citing papers in PubMed, 133 citations in OpenAlex.

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  15. Liver-targeted gene therapy: Approaches and challenges.Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society · 2015
    Review
  16. Article
  17. Targeted genome modification via triple helix formation.Methods in molecular biology (Clifton, N.J.) · 2014
    Article
  18. Article
  19. Article
  20. Inhibition of transcription by platinated triplex-forming oligonucleotides.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2012
    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 3 institutions in 1 country.

A F FaruqiDepartment of Therapeutic Radiology, Yale University School of Medicine, New Haven, Connecticut 06520-8040, USA.
H J Datta
D Carroll
M M Seidman
P M Glazer
Yale University · USNational Institutes of Health · USUniversity of Utah · US

Funding

Gene Targeting Mediated By Triple Helix Forming OligonucleotidesZ01AG000738 · NIA · NATIONAL INSTITUTE ON AGING · PI SEIDMAN, MICHAEL M · 1999 to 2008
$1.4M
RECOMBINATION INDUCED BY TRIPLEX TARGETED DNA DAMAGER01GM054731 · NIGMS · YALE UNIVERSITY · PI GLAZER, PETER M · 1997 to 2004
$1.4M
NIGMS NIH HHS GM54731NIGMS NIH HHS R01 GM054731
6 · The paper itself

Abstract

The ability to stimulate recombination in a site-specific manner in mammalian cells may provide a useful tool for gene knockout and a valuable strategy for gene therapy. We previously demonstrated that psoralen adducts targeted by triple-helix-forming oligonucleotides (TFOs) could induce recombination between tandem repeats of a supF reporter gene in a simian virus 40 vector in monkey COS cells. Based on work showing that triple helices, even in the absence of associated psoralen adducts, are able to provoke DNA repair and cause mutations, we asked whether intermolecular triplexes could stimulate recombination. Here, we report that triple-helix formation itself is capable of promoting recombination and that this effect is dependent on a functional nucleotide excision repair (NER) pathway. Transfection of COS cells carrying the dual supF vector with a purine-rich TFO, AG30, designed to bind as a third strand to a region between the two mutant supF genes yielded recombinants at a frequency of 0.37%, fivefold above background, whereas a scrambled sequence control oligomer was ineffective. In human cells deficient in the NER factor XPA, the ability of AG30 to induce recombination was eliminated, but it was restored in a corrected subline expressing the XPA cDNA. In comparison, the ability of triplex-directed psoralen cross-links to induce recombination was only partially reduced in XPA-deficient cells, suggesting that NER is not the only pathway that can metabolize targeted psoralen photoadducts into recombinagenic intermediates. Interestingly, the triplex-induced recombination was unaffected in cells deficient in DNA mismatch repair, challenging our previous model of a heteroduplex intermediate and supporting a model based on end joining. This work demonstrates that oligonucleotide-mediated triplex formation can be recombinagenic, providing the basis for a potential strategy to direct genome modification by using high-affinity DNA binding ligands.

Indexed as

DNA RepairNucleic Acid ConformationRecombination, GeneticAnimalsBase SequenceCell Line, TransformedChromosome MappingColonic NeoplasmsCOS CellsDNA-Binding ProteinsGenes, ReporterGenes, SuppressorHumansModels, GeneticMutagenesisOligodeoxyribonucleotidesDNA-Binding ProteinsOligodeoxyribonucleotidesRecombinant ProteinsRNA-Binding ProteinsRNA, TransfersupF tRNAXeroderma Pigmentosum Group A ProteinXPA protein, human

Identifiers

PMID10629056
PMCPMC85216
OpenAlexW2125289455

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.