Evidence map›Paper›PMID 21224036›Full record

ReviewThe American journal of pathology2011

Regulation of AMPK by the ubiquitin proteasome system.

Makhosazane Zungu, Jonathan C Schisler, M Faadiel Essop, Chris McCudden, Cam Patterson, Monte S Willis

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. A Mixture ofJournal of microbiology and biotechnology · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Bioactive compounds from Artemisia dracunculus L. activate AMPK signaling in skeletal muscle.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Spatial control of AMPK signaling at subcellular compartments.Critical reviews in biochemistry and molecular biology · 2020
    Review
  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

6 authors at 4 institutions in 2 countries.

Makhosazane ZunguDiscipline of Human Physiology, University of KwaZulu Natal, Durban, South Africa.
Jonathan C Schisler
M Faadiel Essop
Chris McCudden
Cam Patterson
Monte S Willis
Pediatrics and Genetics · USStellenbosch University · ZAUniversity of KwaZulu-Natal · ZAUniversity of North Carolina at Chapel Hill · US

Funding

Myocyte Signaling and the Response to StressR37HL065619 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PATTERSON, WINSTON C · 2010 to 2019
$3.7M
CHIP: A link between the chaperone &proteasome systemsR01GM061728 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SCHISLER, JONATHAN C. · 2001 to 2013
$3.4M
Myocyte specific regulation of metabolism and the response to biomechanical forceR01HL104129 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WILLIS, MONTE S · 2010 to 2018
$3.3M
Myocyte signaling and the response to stressR01HL065619 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PATTERSON, WINSTON C · 2001 to 2009
$2.7M
UNC-Clinician-Scientist Training Program in Cardiovascular MedicineT32HL083828 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI STOUFFER, GEORGE A · 2006 to 2015
$2.0M
NHLBI NIH HHS R01 HL065619NHLBI NIH HHS R01HL065619NHLBI NIH HHS R01 HL104129NHLBI NIH HHS R37 HL065619NHLBI NIH HHS T32 HL083828NIGMS NIH HHS R01 GM061728
6 · The paper itself

Abstract

The 5'-AMP-activated protein kinase (AMPK) functions as a metabolic fuel gauge that is activated in response to environmental stressors to restore cellular energy balance. In the heart, AMPK coordinates the activation of glucose and fatty acid metabolic pathways to ensure increased production of myocardial ATP when required, such as during cardiac ischemia/reperfusion and hypertrophy, causing an increase in AMPK activity that can be viewed as both protective and maladaptive. While we understand the basic regulation of AMPK activity by kinases, recent studies have introduced the concept that AMPK is regulated by other post-translational modifications, specifically ubiquitination. These studies reported that the ubiquitin ligase cell death-inducing DFFA-like effector a ubiquitinates the β subunit of AMPK to regulate its steady-state protein levels. Other investigators found that AMPK regulatory components, including the AMPK α subunit and AMPK kinases NUAK1 and MARK4, can be ubiquitinated with atypical ubiquitin chains. The USP9X-deubiquitinating enzyme was identified to remove ubiquitination from both NUAK1 and MARK4. Lastly, AMPK activation increases the expression of the ubiquitin ligases MAFBx/Atrogin-1 and MuRF1. These ubiquitin ligases regulate key cardiac transcription factors to control cardiomyocyte mass and remodeling, thus suggesting another mechanism by which AMPK may function in the heart. The relevance of AMPK ubiquitination in cardiac disease has yet to be tested directly, but it likely represents an important mechanism that occurs in common cardiac diseases that may be targeted for therapy.

Indexed as

AMP-Activated Protein Kinase KinasesAnimalsHeart DiseasesHumansMiceMuscle ProteinsMyocardiumProteasome Endopeptidase ComplexProtein ConformationProtein KinasesSKP Cullin F-Box Protein LigasesTripartite Motif ProteinsUbiquitinUbiquitinationUbiquitin-Protein LigasesAMP-Activated Protein Kinase KinasesFBXO32 protein, humanMuscle ProteinsProteasome Endopeptidase ComplexProtein KinasesSKP Cullin F-Box Protein LigasesTRIM63 protein, humanTripartite Motif ProteinsUbiquitinUbiquitin-Protein Ligases

Identifiers

PMID21224036
PMCPMC3069915
OpenAlexW2038661349

What Socratic 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 Socratic graph.