Evidence map›Paper›PMID 27226630›Full record

ArticleThe Journal of biological chemistry2016

Unraveling Growth Factor Signaling and Cell Cycle Progression in Individual Fibroblasts.

Sean M Gross, Peter Rotwein

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-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

18 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Genome research · 2024
    Article
  4. Article
  5. Serum-Free Medium Supplemented withFoods (Basel, Switzerland) · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. 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

2 authors at 2 institutions in 1 country.

Sean M GrossFrom the Department of Biochemistry and Molecular Biology, Oregon Health & Science University, Portland, Oregon 97239 and.
Peter Rotweinthe Department of Biomedical Sciences, Paul L. Foster School of Medicine, Texas Tech Health University Health Sciences Center, El Paso, Texas 79905 peter.rotwein@ttuhsc.edu.
Oregon Health & Science University · USTexas Tech University Health Sciences Center · US

Funding

INSULINLIKE GROWTH FACTORS AND MUSCLE DIFFERENTIATIONR01DK042748 · NIDDK · WASHINGTON UNIVERSITY · PI ROTWEIN, PETER S · 1991 to 2017
$5.6M
Training in the Molecular Basis of Skin/Mucosa PathobiologyT32CA106195 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI KULESZ-MARTIN, MOLLY F. · 2004 to 2018
$3.8M
NCI NIH HHS T32 CA106195NIDDK NIH HHS R01 DK042748
6 · The paper itself

Abstract

Cultured cells require the actions of growth factors to enter the cell cycle, but how individual members of a population respond to the same stimulus remains unknown. Here we have employed continuous monitoring by live cell imaging in a dual-reporter cell model to investigate the regulation of short-term growth factor signaling (protein kinase B (PKB/Akt) activity) and longer-term progression through the cell cycle (cyclin-dependent kinase 2 activity). In the total population, insulin-like growth factor-I (IGF-I)-enhanced cell cycle entry by >5-fold compared with serum-free medium (from 13.5 to 78%), but at the single cell level we observed a broad distribution in the timing of G1 exit (4-24 h, mean ∼12 h) that did not vary with either the amount or duration of IGF-I treatment. Cells that failed to re-enter the cell cycle exhibited similar responses to IGF-I in terms of integrated Akt activity and migration distance compared with those that did. We made similar observations with EGF, PDGF-AA, and PDGF-BB. As potential thresholds of growth factor-mediated cell cycle progression appeared to be heterogeneous within the population, the longer-term proliferative outcomes of individual cells to growth factor stimulation could not be predicted based solely on acute Akt signaling responses, no matter how robust these might be. Thus, although we could define a relationship at the population level between growth factor-induced Akt signaling dynamics and cell cycle progression, we could not predict the fate of individual cells.

Indexed as

Cell CycleSignal TransductionAnimalsCell LineCyclin-Dependent Kinase 2Insulin-Like Growth Factor IIntercellular Signaling Peptides and ProteinsMiceProto-Oncogene Proteins c-aktCyclin-Dependent Kinase 2Insulin-Like Growth Factor IIntercellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-aktAkt PKBcell proliferationcell signalinggrowth factorsignal transduction

Identifiers

PMID27226630
PMCPMC4938184
OpenAlexW2389117460

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.