Evidence map›Paper›PMID 19073770›Full record

ArticleDiabetes2009

Gene silencing of phogrin unveils its essential role in glucose-responsive pancreatic beta-cell growth.

Seiji Torii, Naoya Saito, Ayumi Kawano, Ni Hou, Kohjiro Ueki, Rohit N Kulkarni, Toshiyuki Takeuchi

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  4. In focus in HCB.Histochemistry and cell biology · 2024
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  11. X-ray structure of the mature ectodomain of phogrin.Journal of structural and functional genomics · 2015
    Article
  12. Article
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  14. Immunohistochemical analysis of IA-2 family of protein tyrosine phosphatases in rat gastrointestinal endocrine cells.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2013
    Article
  15. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Seiji ToriiSecretion Biology Lab, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.
Naoya Saito
Ayumi Kawano
Ni Hou
Kohjiro Ueki
Rohit N Kulkarni
Toshiyuki Takeuchi
Gunma University · JPHarvard University · USThe University of Tokyo · JP

Funding

Role of IGF-1 and Insulin Receptors Beta-Cell SurvivalR01DK067536 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 2004 to 2026
$8.0M
NIDDK NIH HHS R01 DK067536NIDDK NIH HHS R01-DK-67536
6 · The paper itself

Abstract

objectivePhogrin and IA-2, autoantigens in insulin-dependent diabetes, have been shown to be involved in insulin secretion in pancreatic beta-cells; however, implications at a molecular level are confusing from experiment to experiment. We analyzed biological functions of phogrin in beta-cells by an RNA interference technique. RESEARCH DESIGN AND

methodsAdenovirus-mediated expression of short hairpin RNA specific for phogrin (shPhogrin) was conducted using cultured beta-cell lines and mouse islets. Both glucose-stimulated insulin secretion and cell proliferation rate were determined in the phogrin-knockdown cells. Furthermore, protein expression was profiled in these cells. To see the binding partner of phogrin in beta-cells, coimmunoprecipitation analysis was carried out.

resultsAdenoviral expression of shPhogrin efficiently decreased its endogenous expression in pancreatic beta-cells. Silencing of phogrin in beta-cells abrogated the glucose-mediated mitogenic effect, which was accompanied by a reduction in the level of insulin receptor substrate 2 (IRS2) protein, without any changes in insulin secretion. Phogrin formed a complex with insulin receptor at the plasma membrane, and their interaction was promoted by high-glucose stimulation that in turn led to stabilization of IRS2 protein. Corroboratively, phogrin knockdown had no additional effect on the proliferation of beta-cell line derived from the insulin receptor-knockout mouse.

conclusionsPhogrin is involved in beta-cell growth via regulating stability of IRS2 protein by the molecular interaction with insulin receptor. We propose that phogrin and IA-2 function as an essential regulator of autocrine insulin action in pancreatic beta-cells.

Indexed as

AnimalsAutoantibodiesCell DivisionGene SilencingGenetic VectorsGlucoseInsulinInsulin-Secreting CellsInsulin SecretionMembrane ProteinsMicePromoter Regions, GeneticRabbitsRatsReceptor-Like Protein Tyrosine Phosphatases, Class 8Reverse Transcriptase Polymerase Chain ReactionAutoantibodiesGlucoseICA512 autoantibodyInsulinMembrane Proteinsphogrin protein, mousePtprn protein, mouseReceptor-Like Protein Tyrosine Phosphatases, Class 8RNA Polymerase III

Identifiers

PMID19073770
PMCPMC2646067
OpenAlexW2138179019

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.