Evidence map›Paper›PMID 15024084›Full record

ArticleMolecular and cellular biology2004

Apoptosis associated with deregulated E2F activity is dependent on E2F1 and Atm/Nbs1/Chk2.

Harry A Rogoff, Mary T Pickering, Fiona M Frame, Michelle E Debatis, Yolanda Sanchez, Stephen Jones, Timothy F Kowalik

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

61 citing papers in PubMed, 125 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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  7. Article
  8. E2F1: a promising regulator in ovarian carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Molecular evidence of stress-induced acute heart injury in a mouse model simulating posttraumatic stress disorder.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  14. Genomic Instability and Cancer.Journal of carcinogenesis & mutagenesis · 2014
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Harry A RogoffProgram in Immunology and Virology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
Mary T Pickering
Fiona M Frame
Michelle E Debatis
Yolanda Sanchez
Stephen Jones
Timothy F Kowalik
University of Cincinnati · USUniversity of Massachusetts Chan Medical School · US

Funding

The Role of MDM Proteins in Cell Growth and TumorigenesisR01CA077735 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI JONES, STEPHEN, ZHANG, HONG · 1999 to 2019
$5.7M
TRAINING IN IMMUNOLOGY (COMPETITIVE RENEWAL OF AI07439)T32AI007349 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI STERN, LAWRENCE J. · 1989 to 2024
$4.5M
E2F AND APOPTOSISR01CA086038 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KOWALIK, TIMOTHY F · 2000 to 2004
$1.4M
The Role of MDM Proteins in Cell Growth and TumorigenesisR56CA077735 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI JONES, STEPHEN · 2009 to 2009
$324k
NCI NIH HHS CA77735NCI NIH HHS CA86038NCI NIH HHS R01 CA077735NCI NIH HHS R01 CA086038NCI NIH HHS R56 CA077735NIAID NIH HHS 5T32 AI07349NIAID NIH HHS T32 AI007349
6 · The paper itself

Abstract

The retinoblastoma protein (Rb)/E2F pathway links cellular proliferation control to apoptosis and is critical for normal development and cancer prevention. Here we define a transcription-mediated pathway in which deregulation of E2F1 by ectopic E2F expression or Rb inactivation by E7 of human papillomavirus type 16 signals apoptosis by inducing the expression of Chk2, a component of the DNA damage response. E2F1- and E7-mediated apoptosis are compromised in cells from patients with the related disorders ataxia telangiectasia and Nijmegen breakage syndrome lacking functional Atm and Nbs1 gene products, respectively. Both Atm and Nbs1 contribute to Chk2 activation and p53 phosphorylation following deregulation of normal Rb growth control. E2F2, a related E2F family member that does not induce apoptosis, also activates Atm, resulting in phosphorylation of p53. However, we found that the key commitment step in apoptosis induction is the ability of E2F1, and not E2F2, to upregulate Chk2 expression. Our results suggest that E2F1 plays a central role in signaling disturbances in the Rb growth control pathway and, by upregulation of Chk2, may sensitize cells to undergo apoptosis.

Indexed as

DNA-Binding ProteinsAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCells, CulturedCheckpoint Kinase 2E2F1 Transcription FactorE2F2 Transcription FactorE2F Transcription FactorsFibroblastsGene Expression RegulationHumansMiceMice, TransgenicNuclear ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanAtm protein, mouseCell Cycle ProteinsCheckpoint Kinase 2CHEK2 protein, humanChek2 protein, mouseDNA-Binding ProteinsE2F1 protein, humanE2f1 protein, mouseE2F1 Transcription FactorE2F2 protein, humanE2F2 Transcription FactorE2F Transcription FactorsNBN protein, humanNuclear Proteinsoncogene protein E7, Human papillomavirus type 16Oncogene Proteins, ViralPapillomavirus E7 ProteinsProtein Serine-Threonine KinasesRetinoblastoma ProteinTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID15024084
PMCPMC371110
OpenAlexW2146180420

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.