Evidence map›Paper›PMID 24817119›Full record

ArticleThe Journal of biological chemistry2014

Glucocorticoid receptor β stimulates Akt1 growth pathway by attenuation of PTEN.

Lance A Stechschulte, Leah Wuescher, Joseph S Marino, Jennifer W Hill, Charis Eng, Terry D Hinds

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.3field-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

35 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. FKBP51 and the molecular chaperoning of metabolism.Trends in endocrinology and metabolism: TEM · 2021
    Review
  13. Review
  14. Review
  15. Glucocorticoid Receptor β (GRβ): Beyond Its Dominant-Negative Function.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Active Cushing Disease Is Characterized by Increased Adipose Tissue Macrophage Presence.The Journal of clinical endocrinology and metabolism · 2019
    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 1 country.

Lance A StechschulteFrom the Center for Hypertension and Personalized Medicine, Department of Physiology and Pharmacology and.
Leah Wuescherthe Department of Medical Microbiology and Immunology, University of Toledo College of Medicine, Toledo, Ohio 43614.
Joseph S Marinothe Department of Kinesiology, University of North Carolina at Charlotte, Charlotte, North Carolina 28223.
Jennifer W HillFrom the Center for Hypertension and Personalized Medicine, Department of Physiology and Pharmacology and.
Charis Engthe Genomic Medicine Institute, Lerner Research Institute and Taussig Cancer Institute, Cleveland Clinic, Cleveland, Ohio 44195, and the Department of Genetics and Genome Sciences and CASE Comprehensive Cancer Center, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106.
Terry D HindsFrom the Center for Hypertension and Personalized Medicine, Department of Physiology and Pharmacology and Terry.Hinds@utoledo.edu.
Hypertension Institute · USCase Western Reserve University · USUniversity of North Carolina at Charlotte · USUniversity of Toledo · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Selective Modulation of Thyroidal RadioiodineP01CA124570 · NCI · OHIO STATE UNIVERSITY · PI RINGEL, MATTHEW D · 2008 to 2017
$23.4M
PRIDE: Functional and Translational Genomics of Blood DisordersR25HL106365 · NHLBI · AUGUSTA UNIVERSITY · PI PACE, BETTY SUE · 2010 to 2024
$5.2M
NCI NIH HHS P01 CA124570NHLBI NIH HHS HL106365NHLBI NIH HHS R25 HL106365NIDDK NIH HHS P30 DK020572NIMHD NIH HHS L32 MD009154
6 · The paper itself

Abstract

Glucocorticoids (GCs) are known inhibitors of proliferation and are commonly prescribed to cancer patients to inhibit tumor growth and induce apoptosis via the glucocorticoid receptor (GR). Because of alternative splicing, the GR exists as two isoforms, GRα and GRβ. The growth inhibitory actions of GCs are mediated via GRα, a hormone-induced transcription factor. The GRβ isoform, however, lacks helix 12 of the ligand-binding domain and cannot bind GCs. While we have previously shown that GRβ mRNA is responsive to insulin, the role of GRβ in insulin signaling and growth pathways is unknown. In the present study, we show that GRβ suppresses PTEN expression, leading to enhanced insulin-stimulated growth. These characteristics were independent of the inhibitory qualities that have been reported for GRβ on GRα. Additionally, we found that GRβ increased phosphorylation of Akt basally, which was further amplified following insulin treatment. In particular, GRβ specifically targets Akt1 in growth pathways. Our results demonstrate that the GRβ/Akt1 axis is a major player in insulin-stimulated growth.

Indexed as

3T3-L1 CellsAnimalsGene Expression Regulation, EnzymologicInsulinMiceProtein IsoformsProtein Structure, SecondaryProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseReceptors, GlucocorticoidSignal TransductionAkt1 protein, mouseglucocorticoid receptor betaInsulinProtein IsoformsProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseReceptors, GlucocorticoidAktCell GrowthCell ProliferationGlucocorticoidGlucocorticoid ReceptorHormone ReceptorInsulinPhosphatase and Tensin Homolog (PTEN)

Identifiers

PMID24817119
PMCPMC4067219
OpenAlexW2085617928

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.