Evidence map›Paper›PMID 16897043›Full record

ReviewPflugers Archiv : European journal of physiology2007

ABCC8 and ABCC9: ABC transporters that regulate K+ channels.

Joseph Bryan, Alvaro Muñoz, Xinna Zhang, Martina Düfer, Gisela Drews, Peter Krippeit-Drews, Lydia Aguilar-Bryan

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 2 pooled it
6.3field-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

86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 161 citations in OpenAlex.

  1. Sulfonylurea drugs for people with severe hemispheric ischemic stroke.The Cochrane database of systematic reviews · 2025
    Pooled it
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  11. Differential Expression ofPharmaceutics · 2023
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  16. Sulfonylurea Receptor 1 in Central Nervous System Injury: An Updated Review.International journal of molecular sciences · 2021
    Review
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  18. Article
  19. Article
  20. Review

26 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

7 authors at 2 institutions in 2 countries.

Joseph BryanDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA. jbryan@bcm.tmc.edu
Alvaro Muñoz
Xinna Zhang
Martina Düfer
Gisela Drews
Peter Krippeit-Drews
Lydia Aguilar-Bryan
Baylor College of Medicine · USUniversity of Tübingen · DE

Funding

SULFONYLUREA RECEPTORS AND KATP CHANNELSR01DK044311 · NIDDK · PACIFIC NORTHWEST RESEARCH INSTITUTE · PI BRYAN, JOSEPH · 1994 to 2008
$2.5M
STRUCTURE OF ATP SENSITIVE POTASSIUM CHANNELSR01DK052771 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI BRYAN, JOSEPH · 1997 to 2006
$1.8M
NIDDK NIH HHS DK44311NIDDK NIH HHS DK52771
6 · The paper itself

Abstract

The sulfonylurea receptors (SURs) ABCC8/SUR1 and ABCC9/SUR2 are members of the C-branch of the transport adenosine triphosphatase superfamily. Unlike their brethren, the SURs have no identified transport function; instead, evolution has matched these molecules with K(+) selective pores, either K(IR)6.1/KCNJ8 or K(IR)6.2/KCNJ11, to assemble adenosine triphosphate (ATP)-sensitive K(+) channels found in endocrine cells, neurons, and both smooth and striated muscle. Adenine nucleotides, the major regulators of ATP-sensitive K(+) (K(ATP)) channel activity, exert a dual action. Nucleotide binding to the pore reduces the activity or channel open probability, whereas Mg-nucleotide binding and/or hydrolysis in the nucleotide-binding domains of SUR antagonize this inhibitory action to stimulate channel openings. Mutations in either subunit can alter this balance and, in the case of the SUR1/KIR6.2 channels found in neurons and insulin-secreting pancreatic beta cells, are the cause of monogenic forms of hyperinsulinemic hypoglycemia and neonatal diabetes. Additionally, the subtle dysregulation of K(ATP) channel activity by a K(IR)6.2 polymorphism has been suggested as a predisposing factor in type 2 diabetes mellitus. Studies on K(ATP) channel null mice are clarifying the roles of these metabolically sensitive channels in a variety of tissues.

Indexed as

Amino AcidsAnimalsATP-Binding Cassette TransportersCalciumCatecholaminesCongenital HyperinsulinismDiabetes MellitusDiabetes Mellitus, Type 2Disease Models, AnimalGastric Inhibitory PolypeptideGlucagon-Like Peptide 1GlucoseHumansInfantInfant, NewbornInsulinABCC8 protein, humanAbcc8 protein, mouseABCC9 protein, humanAmino AcidsATP-Binding Cassette TransportersCalciumCatecholaminesGastric Inhibitory PolypeptideGlucagon-Like Peptide 1GlucoseInsulinPotassium ChannelsPotassium Channels, Inwardly RectifyingReceptors, DrugSulfonylurea Receptors

Identifiers

PMID16897043
OpenAlexW2061905525

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.