Evidence map›Paper›PMID 9465026›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Peptide nucleic acid-targeted mutagenesis of a chromosomal gene in mouse cells.

A F Faruqi, M Egholm, P M Glazer

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.3field-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

33 citing papers in PubMed, 139 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Multifunctional Delivery Systems for Peptide Nucleic Acids.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  5. Review
  6. Article
  7. Review
  8. Debugging the genetic code: non-viralCurrent opinion in biomedical engineering · 2018
    Article
  9. Review
  10. Review
  11. Nanotechnology for delivery of peptide nucleic acids (PNAs).Journal of controlled release : official journal of the Controlled Release Society · 2016
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Targeting and processing of site-specific DNA interstrand crosslinks.Environmental and molecular mutagenesis · 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

3 authors at 1 institution in 1 country.

A F FaruqiDepartments of Therapeutic Radiology and Genetics, Yale University School of Medicine, P.O. Box 208040, New Haven, CT 06520-8040, USA.
M Egholm
P M Glazer
Yale University · US

Funding

Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI DAVID L RIMM · 1985 to 2026
$85.0M
TARGETED MUTAGENESIS OF DNA VIA TRIPLE HELIX FORMATIONR01CA064186 · NCI · YALE UNIVERSITY · PI GLAZER, PETER M · 1995 to 2008
$2.6M
NCI NIH HHS CA16359NCI NIH HHS CA64186NCI NIH HHS P30 CA016359NCI NIH HHS R01 CA064186
6 · The paper itself

Abstract

Peptide nucleic acids (PNAs) can bind to single-stranded DNA by Watson-Crick base pairing and can form triple helices via Hoogsteen bonding to DNA/PNA duplexes. A single dimeric PNA molecule can form a clamp via both double- and triple-helix formation. We designed PNAs to bind as clamps to a site in the supFG1 mutation reporter gene carried within a chromosomally integrated, recoverable lambda phage shuttle vector in mouse fibroblasts. The PNAs were introduced into the cells via permeabilization with streptolysin-O, and cellular uptake was confirmed by fluorescein labeling and fluorescent microscopy. PNAs specific for either an 8- or a 10-bp site in the supFG1 gene were found to induce mutations at frequencies in the range of 0.1%, 10-fold above the background. PNAs with three or four mismatches showed poor in vitro target site binding and were ineffective in the mutagenesis assay. No increased mutagenesis was detected with any of the PNAs in the nontargeted cII gene, also carried within the lambda vector, further indicating the specificity of the PNA-induced mutagenesis. DNA sequence analysis revealed that the majority of the mutations were located within the PNA-binding site and consisted mostly of single base pair insertions and deletions within the poly G:C run there, suggesting that a high affinity PNA clamp constitutes a mutagenic lesion that may provoke replication slippage errors. The ability to direct mutations to a target site in chromosomal DNA by using PNAs may provide a useful tool for research and therapeutic applications.

Indexed as

MutagenesisPeptidesAnimalsBacteriophage lambdaCell LineChromosomesDNAGenes, SuppressorHydrogen BondingMiceMice, TransgenicNucleic Acid ConformationOligodeoxyribonucleotidesDNAOligodeoxyribonucleotidesPeptides

Identifiers

PMID9465026
PMCPMC19018
OpenAlexW1967262291

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.