Evidence map›Paper›PMID 15987767›Full record

ArticleAmerican journal of physiology. Cell physiology2005

Role of ubiquitin-proteasome degradation pathway in biogenesis efficiency of {beta}-cell ATP-sensitive potassium channels.

Fei-Fei Yan, Chia-Wei Lin, Etienne A Cartier, Show-Ling Shyng

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 70 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. KFrontiers in endocrinology · 2023
    Review
  7. Subcellular trafficking and endocytic recycling of KAmerican journal of physiology. Cell physiology · 2022
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Molecular and cellular regulation of human glucokinase.Archives of biochemistry and biophysics · 2019
    Review
  13. Article
  14. Article
  15. KATP Channels in the Cardiovascular System.Physiological reviews · 2016
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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 1 institution in 1 country.

Fei-Fei YanCenter for Research on Occupational and Environmental Toxicology, Oregon Health and Science University, 3181 SW Sam Jackson Park Rd., Portland, OR 97239, USA.
Chia-Wei Lin
Etienne A Cartier
Show-Ling Shyng
Oregon Health & Science University · US

Funding

KATP channels and insulin secretionR01DK057699 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI SHYNG, SHOW-LING · 2001 to 2019
$6.1M
NIDDK NIH HHS DK-57699NIDDK NIH HHS R01 DK057699
6 · The paper itself

Abstract

ATP-sensitive potassium (K(ATP)) channels of pancreatic beta-cells mediate glucose-induced insulin secretion by linking glucose metabolism to membrane excitability. The number of plasma membrane K(ATP) channels determines the sensitivity of beta-cells to glucose stimulation. The K(ATP) channel is formed in the endoplasmic reticulum (ER) on coassembly of four inwardly rectifying potassium channel Kir6.2 subunits and four sulfonylurea receptor 1 (SUR1) subunits. Little is known about the cellular events that govern the channel's biogenesis efficiency and expression. Recent studies have implicated the ubiquitin-proteasome pathway in modulating surface expression of several ion channels. In this work, we investigated whether the ubiquitin-proteasome pathway plays a role in the biogenesis efficiency and surface expression of K(ATP) channels. We provide evidence that, when expressed in COS cells, both Kir6.2 and SUR1 undergo ER-associated degradation via the ubiquitin-proteasome system. Moreover, treatment of cells with proteasome inhibitors MG132 or lactacystin leads to increased surface expression of K(ATP) channels by increasing the efficiency of channel biogenesis. Importantly, inhibition of proteasome function in a pancreatic beta-cell line, INS-1, that express endogenous K(ATP) channels also results in increased channel number at the cell surface, as assessed by surface biotinylation and whole cell patch-clamp recordings. Our results support a role of the ubiquitin-proteasome pathway in the biogenesis efficiency and surface expression of beta-cell K(ATP) channels.

Indexed as

Adenosine TriphosphateAnimalsATP-Binding Cassette TransportersChlorocebus aethiopsCOS CellsGene ExpressionIslets of LangerhansKcnj11 ChannelMutationPotassium ChannelsPotassium Channels, Inwardly RectifyingProteasome Endopeptidase ComplexProtein TransportReceptors, DrugSulfonylurea ReceptorsUbiquitinAdenosine TriphosphateATP-Binding Cassette TransportersKcnj11 ChannelPotassium ChannelsPotassium Channels, Inwardly RectifyingProteasome Endopeptidase ComplexReceptors, DrugSulfonylurea ReceptorsUbiquitin

Identifiers

PMID15987767
PMCPMC1350484
OpenAlexW2157399468

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.