Evidence map›Paper›PMID 14585976›Full record

ArticleMolecular and cellular biology2003

Retinoblastoma tumor suppressor: analyses of dynamic behavior in living cells reveal multiple modes of regulation.

Steven P Angus, David A Solomon, Lioba Kuschel, Robert F Hennigan, Erik S Knudsen

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  7. Dynamic as well as stable protein interactions contribute to genome function and maintenance.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2011
    Article
  8. Article
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  11. Partner-regulated interaction of IFN regulatory factor 8 with chromatin visualized in live macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2005
    Article
  12. Article
  13. 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

5 authors at 2 institutions in 2 countries.

Steven P AngusDepartment of Cell Biology, Vontz Center for Molecular Studies, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0521, USA. Steven.Angus@uc.edu
David A Solomon
Lioba Kuschel
Robert F Hennigan
Erik S Knudsen
University of Cincinnati Medical Center · USCarl Zeiss (Germany) · DE

Funding

RB TUMOR SUPPRESSOR--MECHANISMS OF PROLIFERATION CONTROLR01CA082525 · NCI · UNIVERSITY OF CINCINNATI · PI KNUDSEN, ERIK · 1999 to 2003
$1.2M
NCI NIH HHS CA 82525NCI NIH HHS R01 CA082525
6 · The paper itself

Abstract

The retinoblastoma tumor suppressor, RB, assembles multiprotein complexes to mediate cell cycle inhibition. Although many RB binding partners have been suggested to underlie these functions, the validity of these interactions on the behavior of RB complexes in living cells has not been investigated. Here, we studied the dynamic behavior of RB by using green fluorescent protein-RB fusion proteins. Although these proteins were universally nuclear, phosphorylation or oncoprotein binding mediated their active exclusion from the nucleolus. In vivo imaging approaches revealed that RB exists in dynamic equilibrium between a highly mobile and a slower diffusing species, and genetic lesions associated with tumorigenesis increased the fraction of RB in a highly mobile state. The RB complexes dictating cell cycle arrest were surprisingly dynamic and harbored a relatively short residence time on chromatin. In contrast, this rapid exchange was attenuated in cells that are hypersensitive to RB, suggesting that responsiveness may inversely correlate with mobility. The stability of RB dynamics within the cell was additionally modified by the presence and function of critical corepressors. Last, the RB-assembled complexes present in living cells were primarily associated with E2F binding sites in chromatin. In contrast to RB, E2F1 consistently maintained a stable association with E2F sites regardless of cell type. Together, these results elucidate the kinetic framework of RB tumor suppressor action in transcriptional repression and cell cycle regulation.

Indexed as

Cell Cycle ProteinsDNA-Binding ProteinsAnimalsCell CycleCell LineCell MovementCell NucleolusCell NucleusChromatinCyclin-Dependent KinasesCyclin EE2F1 Transcription FactorE2F Transcription FactorsGenes, RetinoblastomaGreen Fluorescent ProteinsHumansCell Cycle ProteinsChromatinCyclin-Dependent KinasesCyclin EDNA-Binding ProteinsE2F1 protein, humanE2f1 protein, ratE2F1 Transcription FactorE2F Transcription FactorsGreen Fluorescent ProteinsLuminescent ProteinsMacromolecular SubstancesRecombinant Fusion ProteinsRepressor ProteinsRetinoblastoma ProteinTranscription Factors

Identifiers

PMID14585976
PMCPMC262398
OpenAlexW2120871109

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.