Evidence map›Paper›PMID 11314026›Full record

ArticleOncogene2001

E2F-1 induces the stabilization of p53 but blocks p53-mediated transactivation.

J Nip, D K Strom, C M Eischen, J L Cleveland, G P Zambetti, S W Hiebert

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Transcription factors that interact with p53 and Mdm2.International journal of cancer · 2016
    Review
  3. Isg15 controls p53 stability and functions.Cell cycle (Georgetown, Tex.) · 2014
    Article
  4. Article
  5. Article
  6. Article
  7. Cell cycle regulator E2F1 modulates angiogenesis via p53-dependent transcriptional control of VEGF.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

6 authors at 4 institutions in 1 country.

J NipDepartment of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
D K Strom
C M Eischen
J L Cleveland
G P Zambetti
S W Hiebert
Vanderbilt University · USSt. Jude Children's Research Hospital · USUniversity of Memphis · USUniversity of Tennessee at Knoxville · US

Funding

Role of AML1-ETO in Acute LeukemiaR01CA064140 · NCI · VANDERBILT UNIVERSITY · PI HIEBERT, SCOTT W · 1994 to 2018
$5.7M
The Bcl-2/Bcl-X Pathway in Myc-Induced LymphomagenesisR01CA076379 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CLEVELAND, JOHN L. · 1998 to 2012
$3.5M
Myc Role in Hematopoiesis, Vasculogenesis &AgiogenesisR01DK044158 · NIDDK · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CLEVELAND, JOHN L. · 1991 to 2009
$2.8M
MUTANT P53 GAIN OF FUNCTION IN TURMORIGENISISR01CA063230 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI ZAMBETTI, GERARD PAUL · 1995 to 2007
$2.3M
TEL AND THE T(12--21) AND B CELL ALLR01CA077274 · NCI · VANDERBILT UNIVERSITY · PI HIEBERT, SCOTT W · 1997 to 2006
$2.1M
E2F AND DIFFERENTIATION, APOPTOSIS, AND LEUKEMIAR01AG013726 · NIA · VANDERBILT UNIVERSITY · PI HIEBERT, SCOTT · 1996 to 2000
$217k
NCI NIH HHS 5 P30 CA27165NCI NIH HHS CA63230NCI NIH HHS CA64140NCI NIH HHS CA76379NCI NIH HHS CA77274NIA NIH HHS AG13726NIDDK NIH HHS DK44158PHS HHS C09346
6 · The paper itself

Abstract

E2F-1 induces p53 accumulation and E2F-1 and p53 form a physical complex, which affects the ability of E2F-1 to activate transcription. We mapped the domains on E2F-1 that interact with p53 and found two p53-binding domains. To understand the functional consequences of the E2F-1/p53 association on p53 activities we identified the domains of E2F-1 that were responsible for the accumulation of p53. Unexpectedly, we found that the E2F-1 transactivation domain was dispensable for p53 induction. By contrast, further deletion of the DP-1 interaction/'marked' box domain eliminated p53 accumulation. Radiolabeling pulse/chase analysis demonstrated that E2F-1 caused post-translational stabilization of p53. Although E2F-1 caused the stabilization of p53, E2F-1 expression impaired p53-dependent transactivation. Thus, the E2F-1 : p53 interaction may provide a checkpoint function to inactivate overactive E2F-1, but the association may also inactivate p53 transactivation to allow cell cycle progression.

Indexed as

Carrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsTranscriptional ActivationAnimalsBinding SitesCell CycleCells, CulturedE2F1 Transcription FactorE2F Transcription FactorsMiceProtein BindingProtein Processing, Post-TranslationalProteinsRetinoblastoma-Binding Protein 1Transcription Factor DP1Arid4a protein, mouseCarrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsE2f1 protein, mouseE2F1 Transcription FactorE2F Transcription FactorsProteinsRetinoblastoma-Binding Protein 1Tfdp1 protein, mouseTranscription Factor DP1Transcription FactorsTumor Suppressor Protein p14ARFTumor Suppressor Protein p53

Identifiers

PMID11314026
OpenAlexW2330982233

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.