Evidence map›Paper›PMID 26038943›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2015

DICER Inactivation Identifies Pancreatic β-Cell "Disallowed" Genes Targeted by MicroRNAs.

Aida Martinez-Sanchez, Marie-Sophie Nguyen-Tu, Guy A Rutter

Open access · hybridAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
10.0field-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

46 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Review
  3. Frontiers in endocrinology · 2025
    Article
  4. Article
  5. Liver kinase B1 (LKB1) regulates the epigenetic landscape of mouse pancreatic beta cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  6. Article
  7. Article
  8. iScience · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. LDHA is enriched in human islet alpha cells and upregulated in type 2 diabetes.Biochemical and biophysical research communications · 2021
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  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

3 authors at 2 institutions in 1 country.

Aida Martinez-SanchezSection of Cell Biology and Functional Genomics, Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Imperial College London, London W12 0NN, United Kingdom.
Marie-Sophie Nguyen-TuSection of Cell Biology and Functional Genomics, Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Imperial College London, London W12 0NN, United Kingdom.
Guy A RutterSection of Cell Biology and Functional Genomics, Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Imperial College London, London W12 0NN, United Kingdom.
Imperial College London · GBGenomics (United Kingdom) · GB

Funding

Medical Research Council GO401641Medical Research Council MR/J0003042/1Medical Research Council MR/K001981/1Wellcome Trust 081958/Z/07/ZWellcome Trust 098424Wellcome Trust WT098424AIA
6 · The paper itself

Abstract

Pancreatic β-cells are the body's sole source of circulating insulin and essential for the maintenance of blood glucose homeostasis. Levels of up to 66 "disallowed" genes, which are strongly expressed and play housekeeping roles in most other mammalian tissues, are unusually low in β-cells. The molecular mechanisms involved in repressing these genes are largely unknown. Here, we explore the role in gene disallowance of microRNAs (miRNAs), a type of small noncoding RNAs that silence gene expression at the posttranscriptional level and are essential for β-cell development and function. To selectively deplete miRNAs from adult β-cells, the miRNA-processing enzyme DICER was inactivated by deletion of the RNase III domain with a tamoxifen-inducible Pdx1CreER transgene. In this model, β-cell dysfunction was apparent 2 weeks after recombination and preceded a decrease in insulin content and loss of β-cell mass. Of the 14 disallowed genes studied, quantitative RT-quantitative real-time PCR revealed that 6 genes (Fcgrt, Igfbp4, Maf, Oat, Pdgfra, and Slc16a1) were up-regulated (1.4- to 2.1-fold, P < .05) at this early stage. Expression of luciferase constructs bearing the 3'-untranslated regions of the corresponding mRNAs in wild-type or DICER-null β-cells demonstrated that Fcgrt, Oat, and Pdgfra are miRNA direct targets. We thus reveal a role for miRNAs in the regulation of disallowed genes in β-cells and provide evidence for a novel means through which noncoding RNAs control the functional identity of these cells independently of actions on β-cell mass.

Indexed as

AnimalsApoptosisGene DeletionGlucoseGlucose IntoleranceHomeodomain ProteinsHyperglycemiaInsulinInsulin-Secreting CellsIntegrasesMice, Inbred C57BLMicroRNAsRibonuclease IIITamoxifenTrans-ActivatorsUp-RegulationCre recombinaseGlucoseHomeodomain ProteinsInsulinIntegrasesMicroRNAspancreatic and duodenal homeobox 1 proteinRibonuclease IIITamoxifenTrans-Activators

Identifiers

PMID26038943
PMCPMC4484783
OpenAlexW1897765507

What OpenQuestion holds

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Registered trials

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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.