Evidence map›Paper›PMID 16954388›Full record

ArticleMolecular and cellular biology2006

A gradient of epidermal growth factor receptor signaling determines the sensitivity of rbf1 mutant cells to E2F-dependent apoptosis.

Nam-Sung Moon, Luisa Di Stefano, Nicholas Dyson

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

45 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Drosophila as a Potential Model for Ocular Tumors.Ocular oncology and pathology · 2015
    Review
  16. Cell death in development: Signaling pathways and core mechanisms.Seminars in cell & developmental biology · 2015
    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

3 authors at 2 institutions in 1 country.

Nam-Sung MoonMassachusetts General Hospital Cancer Research Center, Harvard Medical School, Building 149, Charlestown, MA 02129, USA.
Luisa Di Stefano
Nicholas Dyson
Cancer Research Center · USMassachusetts General Hospital · US

Funding

Screen for genes targeted by homozygous deletion during cancer progressionP01CA095281 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI HABER, DANIEL A. · 2002 to 2006
$8.4M
The E2F/RBF networkR01GM053203 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 1995 to 2010
$4.2M
MUTAGENESIS OF THE PRB POCKET DOMAINR01CA064402 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 1994 to 2015
$4.1M
NCI NIH HHS CA64402NCI NIH HHS P01 CA095281NCI NIH HHS P01CA095281NCI NIH HHS R01 CA064402NIGMS NIH HHS GM53203NIGMS NIH HHS R01 GM053203
6 · The paper itself

Abstract

The inactivation of retinoblastoma (Rb) family members sensitizes cells to apoptosis. This cell death affects the development of mutant animals and also provides a critical constraint to the malignant potential of Rb mutant tumor cells. The extent of apoptosis caused by the inactivation of Rb is highly cell type and tissue specific, but the underlying reasons for this variation are poorly understood. Here, we characterize a specific time and place during Drosophila melanogaster development where rbf1 mutant cells are exquisitely sensitive to apoptosis. During the third larval instar, many rbf1 mutant cells undergo E2F-dependent cell death in the morphogenetic furrow. Surprisingly, this pattern of apoptosis is not caused by inappropriate cell cycle progression but instead involves the action of Argos, a secreted protein that negatively regulates Drosophila epidermal growth factor receptor (EGFR [DER]) activity. Apoptosis of rbf1 mutant cells is suppressed by the activation of DER, ras, or raf or by the inactivation of argos, sprouty, or gap1, and inhibition of DER strongly enhances apoptosis in rbf1 mutant discs. We show that RBF1 and a DER/ras/raf signaling pathway cooperate in vivo to suppress E2F-dependent apoptosis and that the loss of RBF1 alters a normal program of cell death that is controlled by Argos and DER. These results demonstrate that a gradient of DER/ras/raf signaling that occurs naturally during development provides the contextual signals that determine when and where the inactivation of rbf1 results in dE2F1-dependent apoptosis.

Indexed as

ApoptosisSignal TransductionAnimalsAnimals, Genetically ModifiedDrosophila melanogasterDrosophila ProteinsE2F1 Transcription FactorErbB ReceptorsEyeGene Expression RegulationMutationRetinoblastoma ProteinSensitivity and SpecificityTranscription FactorsDrosophila ProteinsE2F1 Transcription FactorErbB ReceptorsRbf protein, DrosophilaRetinoblastoma ProteinTranscription Factors

Identifiers

PMID16954388
PMCPMC1636876
OpenAlexW2051683278

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.