Evidence map›Paper›PMID 25126749›Full record

ArticlePloS one2014

MafA is required for postnatal proliferation of pancreatic β-cells.

Koki Eto, Wataru Nishimura, Hisashi Oishi, Haruhide Udagawa, Miho Kawaguchi, Masaki Hiramoto, Toshiyoshi Fujiwara, Satoru Takahashi, Kazuki Yasuda

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  9. Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
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  13. The prolactin receptor: Diverse and emerging roles in pathophysiology.Journal of clinical & translational endocrinology · 2015
    Review
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Koki EtoDepartment of Metabolic Disorders, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan; Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Wataru NishimuraDepartment of Metabolic Disorders, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Hisashi OishiDepartment of Anatomy and Embryology, Faculty of Medicine, University of Tsukuba, Tennodai, Tsukuba, Ibaraki, Japan.
Haruhide UdagawaDepartment of Metabolic Disorders, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Miho KawaguchiDepartment of Metabolic Disorders, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Masaki HiramotoDepartment of Metabolic Disorders, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Toshiyoshi FujiwaraDepartment of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Satoru TakahashiDepartment of Anatomy and Embryology, Faculty of Medicine, University of Tsukuba, Tennodai, Tsukuba, Ibaraki, Japan.
Kazuki YasudaDepartment of Metabolic Disorders, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
National Center for Global Health and Medicine · JPUniversity of Tsukuba · JPOkayama University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The postnatal proliferation and maturation of insulin-secreting pancreatic β-cells are critical for glucose metabolism and disease development in adults. Elucidation of the molecular mechanisms underlying these events will be beneficial to direct the differentiation of stem cells into functional β-cells. Maturation of β-cells is accompanied by increased expression of MafA, an insulin gene transcription factor. Transcriptome analysis of MafA knockout islets revealed MafA is required for the expression of several molecules critical for β-cell function, including Glut2, ZnT8, Granuphilin, Vdr, Pcsk1 and Urocortin 3, as well as Prolactin receptor (Prlr) and its downstream target Cyclin D2 (Ccnd2). Inhibition of MafA expression in mouse islets or β-cell lines resulted in reduced expression of Prlr and Ccnd2, and MafA transactivated the Prlr promoter. Stimulation of β-cells by prolactin resulted in the phosphorylation and translocation of Stat5B and an increased nuclear pool of Ccnd2 via Prlr and Jak2. Consistent with these results, the loss of MafA resulted in impaired proliferation of β-cells at 4 weeks of age. These results suggest that MafA regulates the postnatal proliferation of β-cells via prolactin signaling.

Indexed as

AnimalsAnimals, NewbornCell LineCell ProliferationCyclin D2Gene ExpressionGene Expression ProfilingGene Expression RegulationGenes, ReporterHumansInsulin-Secreting CellsIslets of LangerhansMaf Transcription Factors, LargeMaleMiceMice, KnockoutCyclin D2Mafa protein, mouseMaf Transcription Factors, LargeReceptors, Prolactin

Identifiers

PMID25126749
PMCPMC4134197
OpenAlexW2012835711

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.