Evidence map›Paper›PMID 9342346›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

Abnormalities of pancreatic islets by targeted expression of a dominant-negative KATP channel.

T Miki, F Tashiro, T Iwanaga, K Nagashima, H Yoshitomi, H Aihara, Y Nitta, T Gonoi, N Inagaki, J i Miyazaki and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
15.6field-weighted citation impact, top 1% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 182 citations in OpenAlex.

  1. Clinical and Genetic Characteristics ofJournal of diabetes research · 2021
    Pooled it
  2. Article
  3. Personalized Therapeutics for KAnnual review of pharmacology and toxicology · 2023
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. The diabetic β-cell: hyperstimulated vs. hyperexcited.Diabetes, obesity & metabolism · 2012
    Review
  17. Article
  18. Review
  19. Nateglinide is Effective for Diabetes Mellitus with Reactive Hypoglycemia in a Child with a Compound Heterozygous ABCC8 Mutation.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2012
    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

11 authors at 3 institutions in 1 country.

T MikiDivision of Molecular Medicine, Center for Biomedical Science, Chiba University School of Medicine, Chuo-ku, Chiba 260, Japan.
F Tashiro
T Iwanaga
K Nagashima
H Yoshitomi
H Aihara
Y Nitta
T Gonoi
N Inagaki
J i Miyazaki
S Seino
Tohoku University · JPChiba University · JPHokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ATP-sensitive K+ (KATP) channels are known to play important roles in various cellular functions, but the direct consequences of disruption of KATP channel function are largely unknown. We have generated transgenic mice expressing a dominant-negative form of the KATP channel subunit Kir6.2 (Kir6.2G132S, substitution of glycine with serine at position 132) in pancreatic beta cells. Kir6.2G132S transgenic mice develop hypoglycemia with hyperinsulinemia in neonates and hyperglycemia with hypoinsulinemia and decreased beta cell population in adults. KATP channel function is found to be impaired in the beta cells of transgenic mice with hyperglycemia. In addition, both resting membrane potential and basal calcium concentrations are shown to be significantly elevated in the beta cells of transgenic mice. We also found a high frequency of apoptotic beta cells before the appearance of hyperglycemia in the transgenic mice, suggesting that the KATP channel might play a significant role in beta cell survival in addition to its role in the regulation of insulin secretion.

Indexed as

MutationPotassium Channels, Inwardly RectifyingAdenosine TriphosphateAmino Acid SequenceAnimalsBlood GlucoseCalciumCations, MonovalentGene TargetingGlucagonImmunohistochemistryInsulinIon Channel GatingIslets of LangerhansMembrane PotentialsMiceAdenosine TriphosphateBlood GlucoseCalciumCations, MonovalentGlucagonInsulinPotassium ChannelsPotassium Channels, Inwardly RectifyingRubidium

Identifiers

PMID9342346
PMCPMC23672
OpenAlexW2034158559

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.