Evidence map›Paper›PMID 20797423›Full record

ArticleMolecular and cellular endocrinology2011

C/EBPβ is AMP kinase sensitive and up-regulates PEPCK in response to ER stress in hepatoma cells.

Mahua Choudhury, Ishtiaq Qadri, Shaikh Mizanoor Rahman, Jill Schroeder-Gloeckler, Rachel C Janssen, Jacob E Friedman

Abstract read
In one paragraph

Article in Molecular and cellular endocrinology, 2011. 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
0.9field-weighted citation impact, top 28% 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, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Experimental model and novel therapeutic targets for non-alcoholic fatty liver disease development.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023
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  5. Article
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  7. RIG-I Deficiency Promotes Obesity-Induced Insulin Resistance.Pharmaceuticals (Basel, Switzerland) · 2021
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Metformin Protects against HMolecular therapy. Nucleic acids · 2018
    Article
  13. Article
  14. Review
  15. Review
  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

6 authors at 1 institution in 1 country.

Mahua ChoudhuryDepartment of Pediatrics, University of Colorado Denver, Aurora, CO 80045, USA.
Ishtiaq Qadri
Shaikh Mizanoor Rahman
Jill Schroeder-Gloeckler
Rachel C Janssen
Jacob E Friedman
University of Colorado Denver · US

Funding

Regulation of Glucose Homestasis by C/EBPBR01DK059767 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI FRIEDMAN, JACOB E · 2000 to 2010
$2.6M
NIDDK NIH HHS R01 DK059767NIDDK NIH HHS R01-DK059767
6 · The paper itself

Abstract

Diabetes and obesity are associated with activation of endoplasmic reticulum (ER) stress; however a direct link between ER stress and increased hepatic gluconeogenesis remains unclear. Here we show that ER stress triggers a significant increase in expression of CCAAT/enhancer-binding protein (C/EBPβ) and phosphorylated CREB together with reduced phospho-AMP-activated protein kinase (pAMPK) in hepatoma cells. ER stress contributed to transcriptional activation of the gluconeogenic phosphoenolpyruvate carboxykinase (PEPCK) promoter in Huh7 and HepG2 cells via cAMP binding motif (CRE site). Chromatin immunoprecipitation assays demonstrate that C/EBPβ is recruited to the PEPCK promoter during ER stress and is reversed by pre-treatment with a JNK inhibitor that relieves ER stress. C/EBPβ but not pCREB was suppressed by the AMPK-activator AICAR or constitutively active AMPK, while dominant negative AMPK increased C/EBPβ expression. These data suggest that ER stress triggers suppression of AMPK while increasing C/EBPβ and pCREB expression which activates PEPCK gene transcription. Understanding how ER stress suppresses AMPK activation and increases C/EBPβ expression could lead to a potentially novel pathway for treatment of diabetes.

Indexed as

Adenylate KinaseAnimalsCarcinoma, HepatocellularCCAAT-Enhancer-Binding Protein-betaCell Line, TumorCyclic AMP Response Element-Binding ProteinEndoplasmic ReticulumEnzyme ActivationGene Expression Regulation, NeoplasticHumansLiver NeoplasmsModels, GeneticPhosphoenolpyruvate Carboxykinase (ATP)Protein BindingProtein Kinase InhibitorsRatsAdenylate KinaseCCAAT-Enhancer-Binding Protein-betaCyclic AMP Response Element-Binding ProteinPhosphoenolpyruvate Carboxykinase (ATP)Protein Kinase InhibitorsThapsigargin

Identifiers

PMID20797423
PMCPMC2981635
OpenAlexW2020529576

What OpenQuestion holds

Textmetadata
LicenceTDM
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.