Evidence map›Paper›PMID 21980072›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2011

Skp2 is required for incretin hormone-mediated β-cell proliferation.

Shuen-Ing Tschen, Senta Georgia, Sangeeta Dhawan, Anil Bhushan

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.8field-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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. The Regulation Role of the Gut-Islets Axis in Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  3. Mechanisms of action of incretin receptor based dual- and tri-agonists in pancreatic islets.American journal of physiology. Endocrinology and metabolism · 2023
    Review
  4. Novel Approaches to Restore Pancreatic Beta-Cell Mass and Function.Handbook of experimental pharmacology · 2022
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Expression of Skp2 and p27Oncology letters · 2015
    Article
  15. Review
  16. Article
  17. Repurposing cAMP-modulating medications to promote β-cell replication.Molecular endocrinology (Baltimore, Md.) · 2014
    Article
  18. Nkx6.1 regulates islet β-cell proliferation via Nr4a1 and Nr4a3 nuclear receptors.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  19. Article
  20. Review
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

4 authors at 1 institution in 1 country.

Shuen-Ing TschenDepartment of Medicine, University of California, Los Angeles, Los Angeles, California 90095-7073, USA.
Senta Georgia
Sangeeta Dhawan
Anil Bhushan
University of California, Los Angeles · US

Funding

Cell Cycle Control Of Beta Cell MassR01DK068763 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BHUSHAN, ANIL · 2004 to 2014
$3.3M
Novel mechanisms to increase beta cell regeneration by p27K01DK088995 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GEORGIA, SENTA K · 2010 to 2012
$414k
NIDDK NIH HHS K01 DK088995NIDDK NIH HHS R01 DK-068763NIDDK NIH HHS R01 DK068763
6 · The paper itself

Abstract

The glucoincretin hormone glucagon-like peptide-1 (GLP-1) and its analog exendin-4 (Ex-4) promote β-cell growth and expansion. Here we report an essential role for Skp2, a substrate recognition component of SCF (Skp, Cullin, F-box) ubiquitin ligase, in promoting glucoincretin-induced β-cell proliferation by regulating the cellular abundance of p27. In vitro, GLP-1 treatment increases Skp2 levels, which accelerates p27 degradation, whereas in vivo, loss of Skp2 prevents glucoincretin-induced β-cell proliferation. Using inhibitors of phosphatidylinositol 3-kinase and Irs2 silencing RNA, we also show that the effects of GLP-1 in facilitating Skp2-dependent p27 degradation are mediated via the Irs2-phosphatidylinositol-3 kinase pathway. Finally, we show that down-regulation of p27 occurs in islets from aged mice and humans, although in these islets, age-dependent accumulation of p16(Ink4a) prevent glucoincretin-induced β-cell proliferation; however, ductal cell proliferation is maintained. Taken together, these data highlight a critical role for Skp2 in glucoincretin-induced β-cell proliferation.

Indexed as

Cell ProliferationAdultAgedAge FactorsAnimalsCells, CulturedCyclin-Dependent Kinase Inhibitor p27ExenatideGene Knockdown TechniquesGlucagon-Like Peptide 1HumansIncretinsInsulin Receptor Substrate ProteinsInsulin-Secreting CellsMiceMice, Inbred C57BLCyclin-Dependent Kinase Inhibitor p27ExenatideGlucagon-Like Peptide 1IncretinsInsulin Receptor Substrate ProteinsIRS2 protein, humanPeptidesPhosphatidylinositol 3-KinasesS-Phase Kinase-Associated ProteinsVenoms

Identifiers

PMID21980072
PMCPMC3231831
OpenAlexW2010195233

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.