Evidence map›Paper›PMID 18303025›Full record

ArticleThe Journal of biological chemistry2008

Targeted gene knock in and sequence modulation mediated by a psoralen-linked triplex-forming oligonucleotide.

Alokes Majumdar, Parameswary A Muniandy, Jia Liu, Ji-lan Liu, Su-ting Liu, Bernard Cuenoud, Michael M Seidman

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. DNA interstrand crosslink repair in mammalian cells: step by step.Critical reviews in biochemistry and molecular biology · 2010
    Review
  19. Review
  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

7 authors at 3 institutions in 2 countries.

Alokes MajumdarLaboratory of Molecular Gerontology, NIA, National Institutes of Health, Baltimore, Maryland 21224, USA.
Parameswary A Muniandy
Jia Liu
Ji-lan Liu
Su-ting Liu
Bernard Cuenoud
Michael M Seidman
National Institutes of Health · USNational Institute on Aging · USNovartis Institutes for BioMedical Research

Funding

Double strand break repairZIAAG000747 · NIA · NATIONAL INSTITUTE ON AGING · PI SEIDMAN, MICHAEL · 2009 to 2010
$320k
Double strand break repairZ01AG000747 · NIA · NATIONAL INSTITUTE ON AGING · PI SEIDMAN, MICHAEL · 2008 to 2008
$258k
Intramural NIH HHS
6 · The paper itself

Abstract

Information from exogenous donor DNA can be introduced into the genome via homology-directed repair (HDR) pathways. These pathways are stimulated by double strand breaks and by DNA damage such as interstrand cross-links. We have employed triple helix-forming oligonucleotides linked to psoralen (pso-TFO) to introduce a DNA interstrand cross-link at a specific site in the genome of living mammalian cells. Co-introduction of duplex DNA with target region homology resulted in precise knock in of the donor at frequencies 2-3 orders of magnitude greater than with donor alone. Knock-in was eliminated in cells deficient in ERCC1-XPF, which is involved in recombinational pathways as well as cross-link repair. Separately, single strand oligonucleotide donors (SSO) were co-introduced with the pso-TFO. These were 10-fold more active than the duplex knock-in donor. SSO efficacy was further elevated in cells deficient in ERCC1-XPF, in contrast to the duplex donor. Resected single strand ends have been implicated as critical intermediates in sequence modulation by SSO, as well as duplex donor knock in. We asked whether there would be a competition between the donor species for these ends if both were present with the pso-TFO. The frequency of duplex donor knock in was unaffected by a 100-fold molar excess of the SSO. The same result was obtained when the homing endonuclease I-SceI was used to initiate HDR at the target site. We conclude that the entry of double strand breaks into distinct HDR pathways is controlled by factors other than the nucleic acid partners in those pathways.

Indexed as

AnimalsBase SequenceCHO CellsCricetinaeCricetulusCross-Linking ReagentsDeoxyribonucleases, Type II Site-SpecificDNA DamageDNA RepairEndonucleasesFicusinHypoxanthine PhosphoribosyltransferaseModels, BiologicalMolecular Sequence DataOligonucleotidesSaccharomyces cerevisiae ProteinsCross-Linking ReagentsDeoxyribonucleases, Type II Site-SpecificEndonucleasesFicusinHypoxanthine PhosphoribosyltransferaseOligonucleotidesSaccharomyces cerevisiae ProteinsSCEI protein, S cerevisiae

Identifiers

PMID18303025
PMCPMC2431054
OpenAlexW2158138924

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.