Evidence map›Paper›PMID 21209369›Full record

ArticleAmerican journal of physiology. Cell physiology2011

Syntaxin 1A regulates surface expression of beta-cell ATP-sensitive potassium channels.

Pei-Chun Chen, Cathrin E Bruederle, Herbert Y Gaisano, Show-Ling Shyng

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Subcellular trafficking and endocytic recycling of KAmerican journal of physiology. Cell physiology · 2022
    Review
  4. Article
  5. Ion Channels of the Islets in Type 2 Diabetes.Journal of molecular biology · 2020
    Review
  6. Plant and Mammal Aquaporins: Same but Different.International journal of molecular sciences · 2018
    Review
  7. Article
  8. Observational
  9. KATP Channels in the Cardiovascular System.Physiological reviews · 2016
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. 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

4 authors at 2 institutions in 2 countries.

Pei-Chun ChenDept. of Biochemistry and Molecular Biology, School of Medicine, Oregon Health & Science Univ., 3181 S. W. Sam Jackson Park Rd., Portland, OR 97239, USA.
Cathrin E Bruederle
Herbert Y Gaisano
Show-Ling Shyng
Oregon Health & Science University · USUniversity of Toronto · CA

Funding

KATP channels and insulin secretionR01DK057699 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI SHYNG, SHOW-LING · 2001 to 2019
$6.1M
NIDDK NIH HHS DK57699NIDDK NIH HHS R01 DK057699
6 · The paper itself

Abstract

The pancreatic ATP-sensitive potassium (K(ATP)) channel consisting of four inwardly rectifying potassium channel 6.2 (Kir6.2) and four sulfonylurea receptor SUR1 subunits plays a key role in insulin secretion by linking glucose metabolism to membrane excitability. Syntaxin 1A (Syn-1A) is a plasma membrane protein important for membrane fusion during exocytosis of insulin granules. Here, we show that Syn-1A and K(ATP) channels endogenously expressed in the insulin-secreting cell INS-1 interact. Upregulation of Syn-1A by overexpression in INS-1 leads to a decrease, whereas downregulation of Syn-1A by small interfering RNA (siRNA) leads to an increase, in surface expression of K(ATP) channels. Using COSm6 cells as a heterologous expression system for mechanistic investigation, we found that Syn-1A interacts with SUR1 but not Kir6.2. Furthermore, Syn-1A decreases surface expression of K(ATP) channels via two mechanisms. One mechanism involves accelerated endocytosis of surface channels. The other involves decreased biogenesis and processing of channels in the early secretory pathway. This regulation is K(ATP) channel specific as Syn-1A has no effect on another inward rectifier potassium channel Kir3.1/3.4. Our results demonstrate that in addition to a previously documented role in modulating K(ATP) channel gating, Syn-1A also regulates K(ATP) channel expression in β-cells. We propose that physiological or pathological changes in Syn-1A expression may modulate insulin secretion by altering glucose-secretion coupling via changes in K(ATP) channel expression.

Indexed as

AnimalsATP-Binding Cassette TransportersCell MembraneChlorocebus aethiopsCOS CellsDown-RegulationEndocytosisGlucoseInsulinInsulin-Secreting CellsInsulin SecretionKATP ChannelsPotassium Channels, Inwardly RectifyingRatsReceptors, DrugRNA InterferenceAbcc8 protein, ratATP-Binding Cassette TransportersGlucoseInsulinKATP ChannelsPotassium Channels, Inwardly RectifyingReceptors, DrugSulfonylurea ReceptorsSyntaxin 1

Identifiers

PMID21209369
PMCPMC3063978
OpenAlexW2018582090

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.