Evidence map›Paper›PMID 17158927›Full record

ArticleMolecular and cellular biology2007

p53-Dependent p21 mRNA elongation is impaired when DNA replication is stalled.

Melissa Mattia, Vanesa Gottifredi, Kristine McKinney, Carol Prives

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Structural Evolution and Dynamics of the p53 Proteins.Cold Spring Harbor perspectives in medicine · 2017
    Review
  10. Article
  11. Article
  12. Article
  13. Challenge to the suppression of tumor growth by the β4-galactosyltransferase genes.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2015
    Review
  14. Article
  15. Article
  16. The p53 circuit board.Biochimica et biophysica acta · 2012
    Review
  17. Article
  18. Article
  19. Article
  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

4 authors at 1 institution in 1 country.

Melissa MattiaDepartment of Biological Sciences, Columbia University, New York, NY 10027, USA.
Vanesa Gottifredi
Kristine McKinney
Carol Prives
Columbia University · US

Funding

Regulation of the p53 tumor suppressor proteinR01CA058316 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI PRIVES, CAROL · 1993 to 2017
$5.3M
REGULATION OF THE P53 TUMOR SUPPRESSOR PROTEINR37CA058316 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI PRIVES, CAROL · 1998 to 2007
$3.8M
NCI NIH HHS CA 58316NCI NIH HHS R01 CA058316NCI NIH HHS R37 CA058316
6 · The paper itself

Abstract

We have previously reported that when DNA replication is blocked in some human cell lines, p53 is impaired in its ability to induce a subset of its key target genes, including p21(WAF1/CIP1). Here, we investigated the reason for this impairment by comparing the effects of two agents, hydroxyurea (HU), which arrests cells in early S phase and impairs induction of p21, and daunorubicin, which causes a G(2) block and leads to robust activation of p21 by p53. HU treatment was shown to inhibit p21 mRNA transcription rather than alter its mRNA stability. Nevertheless, chromatin immunoprecipitation assays revealed that HU impacts neither p53 binding nor acetylation of histones H3 and H4 within the p21 promoter. Furthermore, recruitment of the TFIID/TATA-binding protein complex and the large subunit of RNA polymerase II (RNA Pol II) are equivalent after HU and daunorubicin treatments. Relative to daunorubicin treatment, however, transcription elongation of the p21 gene is significantly impaired in cells treated with HU, as evidenced by reduced occupancy of RNA Pol II at regions downstream of the start site. Likewise, in the p21 downstream region after administration of HU, there is less of a specifically phosphorylated form of RNA Pol II (Pol II-C-terminal domain serine 2P) which occurs only when the polymerase is elongating RNA. We propose that while the DNA replication checkpoint is unlikely to regulate the assembly of a p21 promoter initiation complex, it signals to one or more factors involved in the process of transcriptional elongation.

Indexed as

DNA ReplicationTranscription, GeneticAcetylationCyclin-Dependent Kinase Inhibitor p21DaunorubicinGene Expression Regulation, NeoplasticHCT116 CellsHistonesHumansHydroxyureaPromoter Regions, GeneticProtein BindingProtein TransportRNA, MessengerRNA Polymerase IIRNA StabilityCyclin-Dependent Kinase Inhibitor p21DaunorubicinHistonesHydroxyureaRNA, MessengerRNA Polymerase IITATA-Box Binding ProteinTumor Suppressor Protein p53

Identifiers

PMID17158927
PMCPMC1800727
OpenAlexW2126583463

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.