Evidence map›Paper›PMID 19135240›Full record

ArticleCell2009

Regulation of PKD by the MAPK p38delta in insulin secretion and glucose homeostasis.

Grzegorz Sumara, Ivan Formentini, Stephan Collins, Izabela Sumara, Renata Windak, Bernd Bodenmiller, Reshma Ramracheya, Dorothée Caille, Huiping Jiang, Kenneth A Platt and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed
21.8field-weighted citation impact, top 1% 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

144 citing papers in PubMed, 243 citations in OpenAlex.

  1. Review
  2. p38γ and p38δ MAP kinases in inflammation.Biochemical Society transactions · 2026
    Review
  3. Crinophagy in Pancreatic Beta Cells: From Insulin Granule Turnover to Diabetes Pathogenesis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Protein kinase D1 - A targetable mediator of pancreatic cancer development.Biochimica et biophysica acta. Molecular cell research · 2024
    Review
  15. Article
  16. Metabolic and Molecular Amplification of Insulin Secretion.Advances in anatomy, embryology, and cell biology · 2024
    Review
  17. Article
  18. Article
  19. Article
  20. miR-4431 targets TRIP10/PRKD1 and impairs glucose metabolism.Journal of diabetes investigation · 2022
    Article

84 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 8 institutions in 3 countries.

Grzegorz SumaraInstitute of Cell Biology, ETH Zurich, CH-8093 Zurich, Switzerland.
Ivan Formentini
Stephan Collins
Izabela Sumara
Renata Windak
Bernd Bodenmiller
Reshma Ramracheya
Dorothée Caille
Huiping Jiang
Kenneth A Platt
Paolo Meda
Rudolf Aebersold
Patrik Rorsman
Romeo Ricci
ETH Zurich · CHUniversity of Oxford · GBUniversity of Geneva · CHBoehringer Ingelheim (United States) · USCenter for Pediatric Endocrinology Zurich · CHInstitute for Systems Biology · USLexicon Pharmaceuticals (United States) · USUniversity of Zurich · CH

Funding

Wellcome Trust
6 · The paper itself

Abstract

Dysfunction and loss of insulin-producing pancreatic beta cells represent hallmarks of diabetes mellitus. Here, we show that mice lacking the mitogen-activated protein kinase (MAPK) p38delta display improved glucose tolerance due to enhanced insulin secretion from pancreatic beta cells. Deletion of p38delta results in pronounced activation of protein kinase D (PKD), the latter of which we have identified as a pivotal regulator of stimulated insulin exocytosis. p38delta catalyzes an inhibitory phosphorylation of PKD1, thereby attenuating stimulated insulin secretion. In addition, p38delta null mice are protected against high-fat-feeding-induced insulin resistance and oxidative stress-mediated beta cell failure. Inhibition of PKD1 reverses enhanced insulin secretion from p38delta-deficient islets and glucose tolerance in p38delta null mice as well as their susceptibility to oxidative stress. In conclusion, the p38delta-PKD pathway integrates regulation of the insulin secretory capacity and survival of pancreatic beta cells, pointing to a pivotal role for this pathway in the development of overt diabetes mellitus.

Indexed as

AnimalsExocytosisFemaleGlucoseGolgi ApparatusInsulinInsulin-Secreting CellsInsulin SecretionMaleMiceMitogen-Activated Protein Kinase 13Protein Kinase CType C PhospholipasesGlucoseInsulinMitogen-Activated Protein Kinase 13Protein Kinase Cprotein kinase DType C Phospholipases

Identifiers

PMID19135240
PMCPMC2638021
OpenAlexW2140170107

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.