Evidence map›Paper›PMID 19000992›Full record

ArticleHuman molecular genetics2009

Cx36 makes channels coupling human pancreatic beta-cells, and correlates with insulin expression.

Véronique Serre-Beinier, Domenico Bosco, Laurence Zulianello, Anne Charollais, Dorothée Caille, Eric Charpantier, Benoit R Gauthier, Giuseppe R Diaferia, Ben N Giepmans, Roberto Lupi and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

69 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
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  11. Review
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  13. Review
  14. Article
  15. Pancreatic β-Cell Development and Regeneration.Cold Spring Harbor perspectives in biology · 2022
    Review
  16. Is type 2 diabetes mellitus another intercellular junction-related disorder?Experimental biology and medicine (Maywood, N.J.) · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. Review

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

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

16 authors at 7 institutions in 4 countries.

Véronique Serre-BeinierSurgical Research Unit, Department of Surgery, Geneva University Hospitals, Geneva, Switzerland.
Domenico Bosco
Laurence Zulianello
Anne Charollais
Dorothée Caille
Eric Charpantier
Benoit R Gauthier
Giuseppe R Diaferia
Ben N Giepmans
Roberto Lupi
Piero Marchetti
Shaoping Deng
Léo Buhler
Thierry Berney
Vincenzo Cirulli
Paolo Meda
University of Geneva · CHUniversity Hospital of Geneva · CHUniversity of Pisa · ITCenter for Digestive and Liver Diseases · USScripps Whittier Diabetes Institute · USUniversity of California, San Diego · USUniversity of Pennsylvania · US

Funding

VOLUMETRIC CONTOUR-BASED SURFACE RECONSTRUCTIONP41RR004050 · NCRR · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PASQUALE, ELENA B · 1989 to 2011
$28.0M
PANCREATIC BETA CELL DEVELOPMENT--HUMAN DCC+ STEM CELLSR01DK055183 · NIDDK · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI CIRULLI, VINCENZINO · 1998 to 2002
$841k
NCRR NIH HHS RR4050NIDDK NIH HHS DK55183
6 · The paper itself

Abstract

Previous studies have documented that the insulin-producing beta-cells of laboratory rodents are coupled by gap junction channels made solely of the connexin36 (Cx36) protein, and have shown that loss of this protein desynchronizes beta-cells, leading to secretory defects reminiscent of those observed in type 2 diabetes. Since human islets differ in several respects from those of laboratory rodents, we have now screened human pancreas, and islets isolated thereof, for expression of a variety of connexin genes, tested whether the cognate proteins form functional channels for islet cell exchanges, and assessed whether this expression changes with beta-cell function in islets of control and type 2 diabetics. Here, we show that (i) different connexin isoforms are differentially distributed in the exocrine and endocrine parts of the human pancreas; (ii) human islets express at the transcript level different connexin isoforms; (iii) the membrane of beta-cells harbors detectable levels of gap junctions made of Cx36; (iv) this protein is concentrated in lipid raft domains of the beta-cell membrane where it forms gap junctions; (v) Cx36 channels allow for the preferential exchange of cationic molecules between human beta-cells; (vi) the levels of Cx36 mRNA correlated with the expression of the insulin gene in the islets of both control and type 2 diabetics. The data show that Cx36 is a native protein of human pancreatic islets, which mediates the coupling of the insulin-producing beta-cells, and contributes to control beta-cell function by modulating gene expression.

Indexed as

Gene ExpressionCell MembraneCells, CulturedConnexinsDiabetes Mellitus, Type 2Gap Junction delta-2 ProteinGap JunctionsHumansInsulinInsulin-Secreting CellsIslets of LangerhansPancreasProtein IsoformsConnexinsGap Junction delta-2 ProteinInsulinProtein Isoforms

Identifiers

PMID19000992
PMCPMC2638800
OpenAlexW2136203270

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.