Evidence map›Paper›PMID 26456332›Full record

ArticleCell metabolism2015

Identification of AMPK Phosphorylation Sites Reveals a Network of Proteins Involved in Cell Invasion and Facilitates Large-Scale Substrate Prediction.

Bethany E Schaffer, Rebecca S Levin, Nicholas T Hertz, Travis J Maures, Michael L Schoof, Pablo E Hollstein, Bérénice A Benayoun, Max R Banko, Reuben J Shaw, Kevan M Shokat and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

106 citing papers in PubMed, 182 citations in OpenAlex.

  1. Article
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. The AMPK Pathway: Molecular Rejuvenation of Metabolism and Mitochondria.Annual review of cell and developmental biology · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Energy metabolism in health and diseases.Signal transduction and targeted therapy · 2025
    Review
  18. Article
  19. Article
  20. Article

46 more citing papers are in PubMed but not listed here.

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

11 authors at 4 institutions in 1 country.

Bethany E SchafferCancer Biology Program, Stanford University, Stanford, CA 94305, USA; Department of Genetics, Stanford University, Stanford, CA 94305, USA.
Rebecca S LevinDepartment of Cellular and Molecular Pharmacology, Howard Hughes Medical Institute, University of California, San Francisco, CA 94158, USA.
Nicholas T HertzDepartment of Cellular and Molecular Pharmacology, Howard Hughes Medical Institute, University of California, San Francisco, CA 94158, USA.
Travis J MauresDepartment of Genetics, Stanford University, Stanford, CA 94305, USA.
Michael L SchoofDepartment of Genetics, Stanford University, Stanford, CA 94305, USA.
Pablo E HollsteinMolecular and Cell Biology Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Bérénice A BenayounDepartment of Genetics, Stanford University, Stanford, CA 94305, USA.
Max R BankoDepartment of Genetics, Stanford University, Stanford, CA 94305, USA.
Reuben J ShawMolecular and Cell Biology Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Kevan M ShokatDepartment of Cellular and Molecular Pharmacology, Howard Hughes Medical Institute, University of California, San Francisco, CA 94158, USA.
Anne BrunetCancer Biology Program, Stanford University, Stanford, CA 94305, USA; Department of Genetics, Stanford University, Stanford, CA 94305, USA; Glenn Laboratories for the Biology of Aging, Stanford, CA 94305, USA. Electronic address: abrunet1@stanford.edu.
Stanford University · USHoward Hughes Medical Institute · USSalk Institute for Biological Studies · USUniversity of California, San Francisco · US

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Ye Zheng · 1985 to 2026
$82.8M
Tuberous Sclerosis-Pathway and PathogenesisP01CA120964 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI David J. Kwiatkowski · 2007 to 2026
$35.9M
Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
Bio-Organic Biomedical Mass Spectromy ResourceP41GM103481 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BURLINGAME, ALMA L · 2012 to 2015
$6.4M
TDP-43 Proteinopathies in ALS-DementiaP01AG032953 · NIA · UNIVERSITY OF PENNSYLVANIA · PI LEE, VIRGINIA M · 2010 to 2014
$5.8M
Role of LKB1 and AMPK in Metformin and TZD Control of Glucose Metabolism in LiverR01DK080425 · NIDDK · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI SHAW, REUBEN · 2007 to 2015
$3.6M
Molecular mechanisms underlying lifespan extension by dietary restrictionR01AG031198 · NIA · STANFORD UNIVERSITY · PI BRUNET, ANNE · 2009 to 2013
$2.0M
AMPK and AMPK-related kinases in lung cancer development and treatmentR01CA172229 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI SHAW, REUBEN · 2013 to 2017
$2.0M
LTQ Orbitrap XL ETD Mass SpectrometerS10RR027425 · NCRR · STANFORD UNIVERSITY · PI WANDLESS, THOMAS JAMES · 2010 to 2010
$500k
NCI NIH HHS P01 CA120964NCI NIH HHS P30 CA014195NCI NIH HHS R01 CA172229NCI NIH HHS T32 CA009302NCI NIH HHS T32 CA09302NCRR NIH HHS S10 RR027425NCRR NIH HHS S10RR027425NIA NIH HHS P01-AG032953NIA NIH HHS R01 AG031198NIDDK NIH HHS R01 DK080425NIGMS NIH HHS 8P41GM103481NIGMS NIH HHS P41 GM103481NIGMS NIH HHS P41GM103481
6 · The paper itself

Abstract

AMP-activated protein kinase (AMPK) is a central energy gauge that regulates metabolism and has been increasingly involved in non-metabolic processes and diseases. However, AMPK's direct substrates in non-metabolic contexts are largely unknown. To better understand the AMPK network, we use a chemical genetics screen coupled to a peptide capture approach in whole cells, resulting in identification of direct AMPK phosphorylation sites. Interestingly, the high-confidence AMPK substrates contain many proteins involved in cell motility, adhesion, and invasion. AMPK phosphorylation of the RHOA guanine nucleotide exchange factor NET1A inhibits extracellular matrix degradation, an early step in cell invasion. The identification of direct AMPK phosphorylation sites also facilitates large-scale prediction of AMPK substrates. We provide an AMPK motif matrix and a pipeline to predict additional AMPK substrates from quantitative phosphoproteomics datasets. As AMPK is emerging as a critical node in aging and pathological processes, our study identifies potential targets for therapeutic strategies.

Indexed as

AMP-Activated Protein KinasesAnimalsCell AdhesionCell MovementExtracellular MatrixHumansOncogene ProteinsPeptidesPhosphorylationProtein Interaction MapsSingle-Cell AnalysisSubstrate SpecificityAMP-Activated Protein KinasesNET1 protein, humanOncogene ProteinsPeptides

Identifiers

PMID26456332
PMCPMC4635044
OpenAlexW1775421522

What OpenQuestion holds

Textmetadata
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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.