Evidence map›Paper›PMID 25616257›Full record

ArticleDNA repair2015

A versatile new tool to quantify abasic sites in DNA and inhibit base excision repair.

Shanqiao Wei, Sophia Shalhout, Young-Hoon Ahn, Ashok S Bhagwat

Open access · greenAbstract read
In one paragraph

Article in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Analytical chemistry · 2022
    Article
  8. Article
  9. Detection of Genomic Uracil Patterns.International journal of molecular sciences · 2021
    Review
  10. Article
  11. RNA abasic sites in yeast and human cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. 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

4 authors at 1 institution in 1 country.

Shanqiao WeiDepartment of Chemistry, Wayne State University, Detroit, MI 48202, United States.
Sophia ShalhoutDepartment of Chemistry, Wayne State University, Detroit, MI 48202, United States.
Young-Hoon AhnDepartment of Chemistry, Wayne State University, Detroit, MI 48202, United States.
Ashok S BhagwatDepartment of Chemistry, Wayne State University, Detroit, MI 48202, United States; Department of Immunology and Microbiology, Wayne State University, Detroit, MI 48202, United States. Electronic address: axb@chem.wayne.edu.
Wayne State University · US

Funding

TRANSCRIPTION--INDUCED MUTATIONSR01GM057200 · NIGMS · WAYNE STATE UNIVERSITY · PI BHAGWAT, ASHOK S · 1998 to 2014
$2.6M
NIGMS NIH HHS GM 57200NIGMS NIH HHS R01 GM057200
6 · The paper itself

Abstract

A number of endogenous and exogenous agents, and cellular processes create abasic (AP) sites in DNA. If unrepaired, AP sites cause mutations, strand breaks and cell death. Aldehyde-reactive agent methoxyamine reacts with AP sites and blocks their repair. Another alkoxyamine, ARP, tags AP sites with a biotin and is used to quantify these sites. We have combined both these abilities into one alkoxyamine, AA3, which reacts with AP sites with a better pH profile and reactivity than ARP. Additionally, AA3 contains an alkyne functionality for bioorthogonal click chemistry that can be used to link a wide variety of biochemical tags to AP sites. We used click chemistry to tag AP sites with biotin and a fluorescent molecule without the use of proteins or enzymes. AA3 has a better reactivity profile than ARP and gives much higher product yields at physiological pH than ARP. It is simpler to use than ARP and its use results in lower background and greater sensitivity for AP site detection. We also show that AA3 inhibits the first enzyme in the repair of abasic sites, APE-1, to about the same extent as methoxyamine. Furthermore, AA3 enhances the ability of an alkylating agent, methylmethane sulfonate, to kill human cells and is more effective in such combination chemotherapy than methoxyamine.

Indexed as

DNA DamageAlkynesBiotinCell DeathDNADNA-(Apurinic or Apyrimidinic Site) LyaseDNA Mutational AnalysisDNA RepairHeLa CellsHumansHydroxylaminesMethyl MethanesulfonateSensitivity and SpecificityAlkynesAPEX1 protein, humanBiotinDNADNA-(Apurinic or Apyrimidinic Site) LyaseHydroxylaminesmethoxyamineMethyl MethanesulfonateO-2-propynylhydroxylamineO-(biotinylcarbazoylmethyl)hydroxylamineAbasic sitesAldehyde-reactive probeAP endonucleaseBase excision repairClick chemistryMethoxyamine

Identifiers

PMID25616257
PMCPMC4336807
OpenAlexW2008629383

What OpenQuestion holds

Textmetadata
LicenceTDM
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.