Evidence map›Paper›PMID 27044757›Full record

ArticleJournal of cell science2016

Mapping growth-factor-modulated Akt signaling dynamics.

Sean M Gross, Peter Rotwein

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  7. SDC4-rs1981429 and ATM-rs228590 may provide early biomarkers of breast cancer risk.Journal of cancer research and clinical oncology · 2023
    Article
  8. Article
  9. Engineered combinatorial cell device for wound healing and bone regeneration.Frontiers in bioengineering and biotechnology · 2023
    Article
  10. Article
  11. Article
  12. Analyzing signaling activity and function in hematopoietic cells.The Journal of experimental medicine · 2021
    Review
  13. Review
  14. PI3K in stemness regulation: from development to cancer.Biochemical Society transactions · 2020
    Review
  15. Article
  16. Article
  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

2 authors at 1 institution in 1 country.

Sean M GrossDepartment of Biochemistry and Molecular Biology, Oregon Health & Science University, Portland, OR 97239, USA.
Peter RotweinDepartment of Biochemistry and Molecular Biology, Oregon Health & Science University, Portland, OR 97239, USA Department of Biomedical Sciences, Paul L. Foster School of Medicine, Texas Tech Health University Health Sciences Center, El Paso, TX 79905, USA peter.rotwein@ttuhsc.edu.ORCID 0000-0002-9505-1817
Oregon Health & Science University · 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

Growth factors alter cellular behavior through shared signaling cascades, raising the question of how specificity is achieved. Here, we have determined how growth factor actions are encoded into Akt signaling dynamics by real-time tracking of a fluorescent sensor. In individual cells, Akt activity was encoded in an analog pattern, with similar latencies (∼2 min) and half-maximal peak response times (range of 5-8 min). Yet, different growth factors promoted dose-dependent and heterogeneous changes in signaling dynamics. Insulin treatment caused sustained Akt activity, whereas EGF or PDGF-AA promoted transient signaling; PDGF-BB produced sustained responses at higher concentrations, but short-term effects at low doses, actions that were independent of the PDGF-α receptor. Transient responses to EGF were caused by negative feedback at the receptor level, as a second treatment yielded minimal responses, whereas parallel exposure to IGF-I caused full Akt activation. Small-molecule inhibitors reduced PDGF-BB signaling to transient responses, but only decreased the magnitude of IGF-I actions. Our observations reveal distinctions among growth factors that use shared components, and allow us to capture the consequences of receptor-specific regulatory mechanisms on Akt signaling.

Indexed as

AnimalsBecaplerminCells, CulturedEpidermal Growth FactorGene Expression Regulation, DevelopmentalHeLa CellsHumansInsulinInsulin-Like Growth Factor IOncogene Protein v-aktPhosphatidylinositol 3-KinasesPhosphorylationPlatelet-Derived Growth FactorProto-Oncogene Proteins c-sisSignal TransductionTranscriptional ActivationBecaplerminEpidermal Growth FactorInsulinInsulin-Like Growth Factor IOncogene Protein v-aktPhosphatidylinositol 3-KinasesPlatelet-Derived Growth Factorplatelet-derived growth factor AProto-Oncogene Proteins c-sisAktLive-cell imagingPeptide growth factorsSignaling dynamicsSignaling pathways

Identifiers

PMID27044757
PMCPMC4878993
OpenAlexW2362447271

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.