Evidence map›Paper›PMID 16675953›Full record

ArticleThe EMBO journal2006

A novel leptin signalling pathway via PTEN inhibition in hypothalamic cell lines and pancreatic beta-cells.

Ke Ning, Lisa C Miller, Hilary A Laidlaw, Laura A Burgess, Nevin M Perera, C Peter Downes, Nick R Leslie, Michael L J Ashford

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Article
  3. Mechanisms and Functions of Sweet Reception in Oral and Extraoral Organs.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. Leptin-induced Trafficking of KInternational journal of molecular sciences · 2019
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. PTEN depletion decreases disease severity and modestly prolongs survival in a mouse model of spinal muscular atrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2015
    Article
  18. PTEN function: the long and the short of it.Trends in biochemical sciences · 2014
    Review
  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

8 authors at 2 institutions in 1 country.

Ke NingNeurosciences Institute, Division of Pathology & Neuroscience, Ninewells Hospital & Medical School, University of Dundee, Dundee, UK.
Lisa C Miller
Hilary A Laidlaw
Laura A Burgess
Nevin M Perera
C Peter Downes
Nick R Leslie
Michael L J Ashford
University of Dundee · GBNinewells Hospital · GB

Funding

Medical Research Council G9403619Wellcome Trust 068692
6 · The paper itself

Abstract

In obesity and diabetes, the ability of hypothalamic neurons to sense and transduce changes in leptin and insulin levels is compromised. The effects of both hormones require intracellular signalling via the PI3-kinase pathway, which is inhibited by the phosphatase PTEN. We show that leptin-stimulated F-actin depolymerization in mouse hypothalamic cells is inhibited by PTEN, a process involving independent effects of both its lipid and protein phosphatase activities. Potentially mediating this F-actin depolymerization, leptin, but not insulin, stimulated the phosphorylation of PTEN in a CK2 dependent manner, and inhibited its phosphatase activity. Similarly, hyperpolarization of mouse pancreatic beta-cells by leptin also requires coincident PtdIns(3,4,5)P3 generation and actin depolymerization, and could be inhibited by mechanisms requiring both the lipid and protein phosphatase activities of PTEN. These results demonstrate a critical role for PTEN in leptin signalling and indicate a mechanism by which leptin and insulin can produce PI3K dependent differential cellular outputs.

Indexed as

ActinsAnimalsCells, CulturedHypothalamusInsulin-Secreting CellsLeptinMicePatch-Clamp TechniquesPhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPhosphorylationPotassium ChannelsPTEN PhosphohydrolaseReceptors, Cell SurfaceReceptors, LeptinRNA, Small InterferingActinsLeptinleptin receptor, mousemitochondrial K(ATP) channelphosphatidylinositol 3,4,5-triphosphatePhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPotassium ChannelsPTEN PhosphohydrolasePten protein, mouseReceptors, Cell SurfaceReceptors, LeptinRNA, Small Interfering

Identifiers

PMID16675953
PMCPMC1478173
OpenAlexW1988845013

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.