Evidence map›Paper›PMID 20877711›Full record

ArticlePLoS biology2010

Stochastic E2F activation and reconciliation of phenomenological cell-cycle models.

Tae J Lee, Guang Yao, Dorothy C Bennett, Joseph R Nevins, Lingchong You

Abstract read
In one paragraph

Article in PLoS biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

33 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Cell Cycle Commitment and the Origins of Cell Cycle Variability.Frontiers in cell and developmental biology · 2021
    Review
  7. Review
  8. Article
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  16. Review
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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.

Tae J LeeDepartment of Biomedical Engineering, Duke University, Durham, North Carolina, United States of America.
Guang Yao
Dorothy C Bennett
Joseph R Nevins
Lingchong You

Funding

Project 6P50GM081883 · NIGMS · DUKE UNIVERSITY · PI BENFEY, PHILIP N · 2007 to 2012
$14.9M
Molecular Mechanisms of E2F SpecificityR01CA104663 · NCI · DUKE UNIVERSITY · PI NEVINS, JOSEPH R · 2003 to 2012
$3.4M
Howard Hughes Medical InstituteNCI NIH HHS R01 CA104663NIGMS NIH HHS 1P50GM081883NIGMS NIH HHS P50 GM081883
6 · The paper itself

Abstract

The transition of the mammalian cell from quiescence to proliferation is a highly variable process. Over the last four decades, two lines of apparently contradictory, phenomenological models have been proposed to account for such temporal variability. These include various forms of the transition probability (TP) model and the growth control (GC) model, which lack mechanistic details. The GC model was further proposed as an alternative explanation for the concept of the restriction point, which we recently demonstrated as being controlled by a bistable Rb-E2F switch. Here, through a combination of modeling and experiments, we show that these different lines of models in essence reflect different aspects of stochastic dynamics in cell cycle entry. In particular, we show that the variable activation of E2F can be described by stochastic activation of the bistable Rb-E2F switch, which in turn may account for the temporal variability in cell cycle entry. Moreover, we show that temporal dynamics of E2F activation can be recast into the frameworks of both the TP model and the GC model via parameter mapping. This mapping suggests that the two lines of phenomenological models can be reconciled through the stochastic dynamics of the Rb-E2F switch. It also suggests a potential utility of the TP or GC models in defining concise, quantitative phenotypes of cell physiology. This may have implications in classifying cell types or states.

Indexed as

Cell CycleModels, BiologicalStochastic ProcessesAnimalsBlotting, WesternCell LineE2F Transcription FactorsFlow CytometryRatsE2F Transcription Factors

Identifiers

PMID20877711
PMCPMC2943438

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Registered trials

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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.