Evidence map›Paper›PMID 10468580›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Syntaxin 1 interacts with the L(D) subtype of voltage-gated Ca(2+) channels in pancreatic beta cells.

S N Yang, O Larsson, R Bränström, A M Bertorello, B Leibiger, I B Leibiger, T Moede, M Köhler, B Meister, P O Berggren

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.3field-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

51 citing papers in PubMed, 138 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Enhanced expression of β cell CaProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  5. CaProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  6. Review
  7. Diet-induced β-cell insulin resistance results in reversible loss of functional β-cell mass.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Ionic mechanisms in pancreatic β cell signaling.Cellular and molecular life sciences : CMLS · 2014
    Review
  14. Article
  15. Article
  16. Pancreatic function, type 2 diabetes, and metabolism in aging.International journal of endocrinology · 2012
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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

10 authors at 1 institution in 1 country.

S N YangThe Rolf Luft Center for Diabetes Research, Department of Molecular Medicine, Karolinska Institutet, Karolinska Hospital, S-171 76 Stockholm, Sweden.
O Larsson
R Bränström
A M Bertorello
B Leibiger
I B Leibiger
T Moede
M Köhler
B Meister
P O Berggren
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interaction of syntaxin 1 with the alpha(1D) subunit of the voltage-gated L type Ca(2+) channel was investigated in the pancreatic beta cell. Coexpression of the enhanced green fluorescent protein-linked alpha(1D) subunit with the enhanced blue fluorescent protein-linked syntaxin 1 and Western blot analysis together with subcellular fractionation demonstrated that the alpha(1D) subunit and syntaxin 1 were colocalized in the plasma membrane. Furthermore, the alpha(1D) subunit was coimmunoprecipitated efficiently by a polyclonal antibody against syntaxin 1. Syntaxin 1 also played a central role in the modulation of L type Ca(2+) channel activity because there was a faster Ca(2+) current run-down in cells incubated with antisyntaxin 1 compared with controls. In parallel, antisyntaxin 1 markedly reduced insulin release in both intact and permeabilized cells, subsequent to depolarization with K(+) or exposure to high Ca(2+). Exchanging Ca(2+) for Ba(2+) abolished the effect of antisyntaxin 1 on both Ca(2+) channel activity and insulin exocytosis. Moreover, antisyntaxin 1 had no significant effects on Ca(2+)-independent insulin release trigged by hypertonic stimulation. This suggests that there is a structure-function relationship between the alpha(1D) subunit of the L type Ca(2+) channel and the exocytotic machinery in the pancreatic beta cell.

Indexed as

AnimalsAntibodies, MonoclonalAntigens, SurfaceCalciumCalcium ChannelsCalcium Channels, L-TypeCell MembraneCentrifugation, Density GradientExocytosisGreen Fluorescent ProteinsIslets of LangerhansLuminescent ProteinsMacromolecular SubstancesMiceMice, ObeseNerve Tissue ProteinsAntibodies, MonoclonalAntigens, SurfaceCalciumCalcium ChannelsCalcium Channels, L-TypeGreen Fluorescent ProteinsLuminescent ProteinsMacromolecular SubstancesNerve Tissue ProteinsRecombinant Fusion ProteinsStx1a protein, mouseSyntaxin 1Tubulin

Identifiers

PMID10468580
PMCPMC17860
OpenAlexW2066402939

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.