Evidence map›Paper›PMID 10958668›Full record

ArticleMolecular and cellular biology2000

Characterization of the role of AMP-activated protein kinase in the regulation of glucose-activated gene expression using constitutively active and dominant negative forms of the kinase.

A Woods, D Azzout-Marniche, M Foretz, S C Stein, P Lemarchand, P Ferré, F Foufelle, D Carling

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
6.7field-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

137 citing papers in PubMed, 403 citations in OpenAlex.

  1. Article
  2. Article
  3. Role of AMPKZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. The AMPK/p27Cells · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Anti-inflammatory Property of AMP-activated Protein Kinase.Anti-inflammatory & anti-allergy agents in medicinal chemistry · 2020
    Review
  18. Article
  19. Article
  20. Article

77 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

8 authors at 3 institutions in 2 countries.

A WoodsCellular Stress Group, MRC Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom.
D Azzout-Marniche
M Foretz
S C Stein
P Lemarchand
P Ferré
F Foufelle
D Carling
Inserm · FRHammersmith Hospital · GBCentre de Recherche des Cordeliers · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the liver, glucose induces the expression of a number of genes involved in glucose and lipid metabolism, e.g., those encoding L-type pyruvate kinase and fatty acid synthase. Recent evidence has indicated a role for the AMP-activated protein kinase (AMPK) in the inhibition of glucose-activated gene expression in hepatocytes. It remains unclear, however, whether AMPK is involved in the glucose induction of these genes. In order to study further the role of AMPK in regulating gene expression, we have generated two mutant forms of AMPK. One of these (alpha1(312)) acts as a constitutively active kinase, while the other (alpha1DN) acts as a dominant negative inhibitor of endogenous AMPK. We have used adenovirus-mediated gene transfer to express these mutants in primary rat hepatocytes in culture in order to determine their effect on AMPK activity and the transcription of glucose-activated genes. Expression of alpha1(312) increased AMPK activity in hepatocytes and blocked completely the induction of a number of glucose-activated genes in response to 25 mM glucose. This effect is similar to that observed following activation of AMPK by 5-amino-imidazolecarboxamide riboside. Expression of alpha1DN markedly inhibited both basal and stimulated activity of endogenous AMPK but had no effect on the transcription of glucose-activated genes. Our results suggest that AMPK is involved in the inhibition of glucose-activated gene expression but not in the induction pathway. This study demonstrates that the two mutants we have described will provide valuable tools for studying the wider physiological role of AMPK.

Indexed as

Gene Expression Regulation, EnzymologicAcetyl-CoA CarboxylaseAmino Acid SequenceAMP-Activated Protein KinasesAnimalsCell LineFatty Acid SynthasesFemaleGlucoseHumansLiverMolecular Sequence DataMultienzyme ComplexesNuclear ProteinsProteinsProtein Serine-Threonine KinasesAcetyl-CoA CarboxylaseAMP-Activated Protein KinasesFatty Acid SynthasesGlucoseMultienzyme ComplexesNuclear ProteinsPRKAA1 protein, humanProteinsProtein Serine-Threonine KinasesPyruvate KinaseTHRSP protein, humanThrsp protein, ratTranscription Factors

Identifiers

PMID10958668
PMCPMC86183
OpenAlexW2134535786

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.