Evidence map›Paper›PMID 18281289›Full record

ArticleThe Journal of biological chemistry2008

Multiple mechanisms contribute to inhibit transcription in response to DNA damage.

George F Heine, Andrew A Horwitz, Jeffrey D Parvin

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 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

37 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Dynamic Supercoiling Sponsors Transcription Amplification by MYC.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. IncRNA-ZFAS1, an Emerging Gate-Keeper in DNA Damage-Dependent Transcriptional Regulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. DNA damage reduces heterogeneity and coherence of chromatin motions.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  13. Review
  14. Article
  15. Deficiency in classical nonhomologous end-joining-mediated repair of transcribed genes is linked to SCA3 pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  16. Article
  17. AFF1 acetylation by p300 temporally inhibits transcription during genotoxic stress response.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  18. Review
  19. Article
  20. Structure and function of the histone chaperone FACT - Resolving FACTual issues.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018
    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

3 authors at 2 institutions in 1 country.

George F HeineDepartment of Biomedical Informatics and the Comprehensive Cancer Center, Ohio State University, Columbus, OH 43210, USA.
Andrew A Horwitz
Jeffrey D Parvin
Harvard University · USThe Ohio State University · US

Funding

BRCA1 FunctionR01CA090281 · NCI · OHIO STATE UNIVERSITY · PI PARVIN, JEFFREY D · 2002 to 2006
$1.7M
Understanding the role of BRCA1 in response to DNA damageF32CA130302 · NCI · OHIO STATE UNIVERSITY · PI HEINE, GEORGE F · 2007 to 2009
$148k
NCI NIH HHS CA 130302NCI NIH HHS CA 90281
6 · The paper itself

Abstract

Cellular DNA damage elicits the phosphorylation and ubiquitination of RNA polymerase II (RNAPII), leading to the global repression of transcription. In this report we show that there are at least two different pathways to transcriptional repression, depending on the type of DNA damage. After H2O2 treatment, transcription was rapidly inhibited and rapidly restored. On the other hand, UV irradiation caused a much slower transcriptional inhibition, with a corresponding depletion of unphosphorylated RNAPII. We found that after UV treatment, but not treatment with H2O2, the inhibition of transcription was dependent on both the proteasome and new protein synthesis. In addition, RNAPII activity and ubiquitination were regulated through the phosphorylation of RNAPII by the P-TEFb kinase. These results highlight that multiple cellular pathways exist to globally repress transcriptional processes that might interfere with the repair of DNA damage.

Indexed as

Ultraviolet RaysDNA DamageDNA RepairHeLa CellsHumansHydrogen PeroxideOxidantsPhosphorylationProteasome Endopeptidase ComplexProtein BiosynthesisRNA Polymerase IITranscription, GeneticUbiquitinationHydrogen PeroxideOxidantsProteasome Endopeptidase ComplexRNA Polymerase II

Identifiers

PMID18281289
PMCPMC2442283
OpenAlexW2023143197

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.