Evidence map›Paper›PMID 18669632›Full record

ArticleThe Journal of biological chemistry2008

Differential blocking effects of the acetaldehyde-derived DNA lesion N2-ethyl-2'-deoxyguanosine on transcription by multisubunit and single subunit RNA polymerases.

Tsu-Fan Cheng, Xiaopeng Hu, Averell Gnatt, Philip J Brooks

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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. DNA Polymerase η Promotes the Transcriptional Bypass ofJournal of the American Chemical Society · 2021
    Article
  6. Article
  7. Effects of acetaldehyde-induced DNA lesions on DNA metabolism.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2020
    Article
  8. Mechanism of DNA alkylation-induced transcriptional stalling, lesion bypass, and mutagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
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 2 institutions in 1 country.

Tsu-Fan ChengSection on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892.
Xiaopeng HuDepartment of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore, Maryland 21201.
Averell GnattDepartment of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore, Maryland 21201.
Philip J BrooksSection on Molecular Neurobiology, Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892. Electronic address: pjbrooks@mail.nih.gov.
National Institute on Alcohol Abuse and Alcoholism · USUniversity of Maryland, Baltimore · US

Funding

The role of DNA damage in human disease: Neurodegeneration and CancerZ01AA000083 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI BROOKS, PHILIP J · 1994 to 2008
$2.3M
The role of DNA damage in human disease: Neurodegeneration and CancerZIAAA000083 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI BROOKS, PHILIP J · 2009 to 2011
$1.8M
Intramural NIH HHS
6 · The paper itself

Abstract

Acetaldehyde, the first metabolite of ethanol, reacts with DNA to form adducts, including N(2)-ethyl-2'-deoxyguanosine (N(2)-Et-dG). Although the effects of N(2)-Et-dG on DNA polymerases have been well studied, nothing is known about possible effects of this lesion on transcription by RNA polymerases (RNAPs). Using primer extension assays in vitro, we found that a single N(2)-Et-dG lesion is a strong block to both mammalian RNAPII and two other multisubunit RNAPs, (yeast RNAPII and Escherichia coli RNAP), as well as to T7 RNAP. However, the mechanism of transcription blockage appears to differ between the multisubunit RNAPs and T7 RNAP. Specifically, all three of the multisubunit RNAPs can incorporate a single rNTP residue opposite the lesion, whereas T7 RNAP is essentially unable to do so. Using the mammalian RNAPII, we found that CMP is exclusively incorporated opposite the N(2)-Et-dG lesion. In addition, we also show that the accessory transcription factor TFIIS does not act as a lesion bypass factor, as it does for other nonbulky DNA lesions; instead, it stimulates the polymerase to remove the CMP incorporated opposite the lesion by mammalian RNAPII. We also include models of the N(2)-Et-dG within the active site of yeast RNAPII, which are compatible with our observations.

Indexed as

AnimalsBacteriophage T7CattleDeoxyguanosineDNADNA-Directed RNA PolymerasesEscherichia coliEscherichia coli ProteinsRNA Polymerase IISaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranscriptional Elongation FactorsTranscription, GeneticViral Proteinsbacteriophage T7 RNA polymeraseDeoxyguanosineDNADNA-Directed RNA PolymerasesEscherichia coli ProteinsN2-ethyl-2'-deoxyguanosineRNA Polymerase IISaccharomyces cerevisiae ProteinsTranscriptional Elongation Factorstranscription factor S-IIViral Proteins

Identifiers

PMID18669632
PMCPMC3762520
OpenAlexW2163724411

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.