Evidence map›Paper›PMID 16186129›Full record

ArticleNucleic acids research2005

Triplex targeted genomic crosslinks enter separable deletion and base substitution pathways.

Sally Richards, Su-Ting Liu, Alokes Majumdar, Ji-Lan Liu, Rodney S Nairn, Michel Bernier, Veronica Maher, Michael M Seidman

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. DNA cross-link induced by trans-4-hydroxynonenal.Environmental and molecular mutagenesis · 2010
    Review
  10. Targeting and processing of site-specific DNA interstrand crosslinks.Environmental and molecular mutagenesis · 2010
    Review
  11. A novel link to base excision repair?Trends in biochemical sciences · 2010
    Article
  12. DNA interstrand crosslink repair in mammalian cells: step by step.Critical reviews in biochemistry and molecular biology · 2010
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 1 institution in 1 country.

Sally RichardsLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Dr, Baltimore, MD 21224, USA.
Su-Ting Liu
Alokes Majumdar
Ji-Lan Liu
Rodney S Nairn
Michel Bernier
Veronica Maher
Michael M Seidman
National Institute on Aging · US

Funding

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
Gene Targeting Mediated By Triple Helix Forming OligonucleotidesZ01AG000738 · NIA · NATIONAL INSTITUTE ON AGING · PI SEIDMAN, MICHAEL M · 1999 to 2008
$1.4M
Intramural NIH HHSNCI NIH HHS CA097175NCI NIH HHS P01 CA097175
6 · The paper itself

Abstract

We have synthesized triple helix forming oligonucleotides (TFOs) that target a psoralen (pso) interstrand crosslink to a specific chromosomal site in mammalian cells. Mutagenesis of the targeted crosslinks results in base substitutions and deletions. Identification of the gene products involved in mutation formation is important for developing practical applications of pso-TFOs, and may be informative about the metabolism of other interstrand crosslinks. We have studied mutagenesis of a pso-TFO genomic crosslink in repair proficient and deficient cells. Deficiencies in non homologous end joining and mismatch repair do not influence mutation patterns. In contrast, the frequency of base substitutions is dependent on the activity of ERCC1/XPF and polymerase zeta, but independent of other nucleotide excision repair (NER) or transcription coupled repair (TCR) genes. In NER/TCR deficient cells the frequency of deletions rises, indicating that in wild-type cells NER/TCR functions divert pso-TFO crosslinks from processes that result in deletions. We conclude that targeted pso-TFO crosslinks can enter genetically distinct mutational routes that resolve to base substitutions or deletions.

Indexed as

MutagenesisSequence DeletionAnimalsBase SequenceCHO CellsCricetinaeCricetulusCross-Linking ReagentsDNADNA-Binding ProteinsDNA-Directed DNA PolymeraseDNA RepairFicusinG1 PhaseGenomicsHumansCross-Linking ReagentsDNADNA-Binding ProteinsDNA-Directed DNA PolymeraseDNA polymerase zetaFicusinHypoxanthine PhosphoribosyltransferaseOligonucleotidestriplex DNAxeroderma pigmentosum group F protein

Identifiers

PMID16186129
PMCPMC1236719
OpenAlexW1970176850

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.