Cited by 107Pancreatic function and diabetesIon channel regulation and functionIon Transport and Channel Regulation

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

ATP-sensitive K + channels and disease: from molecule to malady

Ashcroft, Frances M.·2007·American Journal of Physiology-Endocrinology and Metabolism

DOI 10.1152/ajpendo.00348.2007

Open this paper in CoChat — free account

Abstract

This essay is based on a lecture given to the American Physiological Society in honor of Walter B. Cannon, an advocate of homeostasis. It focuses on the role of the ATP-sensitive potassium K(+) (K(ATP)) channel in glucose homeostasis and, in particular, on its role in insulin secretion from pancreatic beta-cells. The beta-cell K(ATP) channel comprises pore-forming Kir6.2 and regulatory SUR1 subunits, and mutations in either type of subunit can result in too little or too much insulin release. Here, I review the latest information on the relationship between K(ATP) channel structure and function, and consider how mutations in the K(ATP) channel genes lead to neonatal diabetes or congenital hyperinsulinism.

Integrity signals

Registry

Crossref · 10.1152/ajpendo.00348.2007

Cites

0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

A genome-wide association study identifies novel risk loci for type 2 diabetes
Sladek, R., Rocheleau, G., Rung, J., Dina, C., Shen, L., Serre, D., Boutin, P., Vincent, D., Belisle, A., Hadjadj, S., et al. (2007) · Nature · doi:10.1038/nature05616 · Cited by 2,993
Replication of Genome-Wide Association Signals in UK Samples Reveals Risk Loci for Type 2 Diabetes
Zeggini, E., Weedon, M. N., Lindgren, C. M., Frayling, T. M., Elliott, K. S., Lango, H., Timpson, N. J., Perry, J. R. B., Rayner, N. W., Freathy, R. M., et al. (2007) · Science · doi:10.1126/science.1142364 · Cited by 2,194
Intracellular ATP directly blocks K+ channels in pancreatic B-cells
Cook, D. L., & Hales, N. (1984) · Nature · doi:10.1038/311271a0 · Cited by 1,208 · cited 3×
“A similar KATP channel had also just been described by Dan Cook and Nick Hales in inside-out patches excised from pancreatic -cells (10).”
BackgroundMethod
Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes
Gloyn, A. L., Pearson, E. R., Antcliff, J. F., Proks, P., Bruining, G. J., Slingerland, A. S., Howard, N., Srinivasan, S., Silva, J. M. C. L., Molnes, J., et al. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa032922 · Cited by 1,137
Self-citation
Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations
Pearson, E. R., Flechtner, I., Njølstad, P. R., Malecki, M. T., Flanagan, S. E., Larkin, B., Ashcroft, F. M., Klimes, I., Codner, E., Iotova, V., et al. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa061759 · Cited by 988
Self-citation
Large-Scale Association Studies of Variants in Genes Encoding the Pancreatic β-Cell KATP Channel Subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) Confirm That the KCNJ11 E23K Variant Is Associated With Type 2 Diabetes
Gloyn, A. L., Weedon, M. N., Owen, K. R., Turner, M. J., Knight, B. A., Hitman, G., Walker, M., Levy, J. C., Sampson, M., Halford, S., et al. (2003) · Diabetes · doi:10.2337/diabetes.52.2.568 · Cited by 754
Activating Mutations in the ABCC8 Gene in Neonatal Diabetes Mellitus
Babenko, A. P., Polak, M., Cavé, H., Busiah, K., Czernichow, P., Scharfmann, R., Bryan, J., Aguilar-Bryan, L., Vaxillaire, M., & Froguel, P. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa055068 · Cited by 655
Glucose dependent K+-channels in pancreatic?-cells are regulated by intracellular ATP
Rorsman, P., & Trube, G. (1985) · Pfl�gers Archiv European Journal of Physiology · doi:10.1007/bf00595682 · Cited by 387
Sulphonylurea action revisited: the post-cloning era
Gribble, F. M., & Reimann, F. (2003) · Diabetologia · doi:10.1007/s00125-003-1143-3 · Cited by 284
The Changes in Adenine Nucleotides Measured in Glucose-stimulated Rodent Islets Occur in β Cells but Not in α Cells and Are Also Observed in Human Islets
Detimary, P., Dejonghe, S., Ling, Z., Pipeleers, D., Schuit, F., & Henquin, J.-C. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.51.33905 · Cited by 159 · cited 1×
“to 4 mM when glucose is increased from 0 to 10 mM (11, 84).”
Background

Flagged first, then by citations

Show all 0 references

Research works printed but not linked: 82

10.1126/science.7716547 · DOI · Paper page
10.1038/sj.emboj.7600487 · DOI
10.1172/JCI25495 · DOI
10.1038/312446a0 · DOI · Paper page
10.1113/jphysiol.1989.sp017765 · DOI
10.1016/0079-6107(89)90013-8 · DOI
10.1007/BF01228295 · DOI
10.1016/S0006-2952(00)00267-7 · DOI
10.1056/NEJM199309303291401 · DOI · Paper page
10.1152/physrev.00022.2003 · DOI
10.1016/0014-5793(86)81532-0 · DOI · Paper page
Edghill EL , Gloyn AL, Gillespie KM, Lambert AP, Raymond NT, Swift PG, Ellard S, Gale EA, Hattersley AT. Activating mutations in the KCNJ11 gene encoding the ATP-sensitive K+ channel subunit Kir6.2 are rare in clinically defined type 1 diabetes diagnosed before 2 years. Diabetes 5 : 2998–3001, 2004. · DOI
10.1086/519174 · DOI · Paper page
10.1074/jbc.272.9.5388 · DOI
10.1016/j.yjmcc.2005.01.005 · DOI
10.2337/db07-0043 · DOI
10.1126/science.1141634 · DOI · Paper page
10.1007/s00424-006-0112-3 · DOI
10.1002/humu.10277 · DOI
10.1002/humu.20292 · DOI
10.1074/jbc.273.41.26383 · DOI · Paper page
10.1093/emboj/16.6.1145 · DOI · Paper page
10.1073/pnas.95.12.7185 · DOI · Paper page
10.1016/j.yjmcc.2005.01.007 · DOI
10.1007/BF00656997 · DOI · Paper page
10.2337/diabetes.54.9.2503 · DOI
10.1038/271271a0 · DOI
10.1007/BF00401417 · DOI
10.1007/BF01971450 · DOI · Paper page
10.1016/S0140-6736(03)12325-2 · DOI
10.1126/science.270.5239.1166 · DOI · Paper page
10.1016/S0014-5793(97)00488-2 · DOI
10.1016/j.yjmcc.2005.02.026 · DOI
10.1016/0014-5793(86)81533-2 · DOI · Paper page
10.1016/S0014-5793(96)01438-X · DOI
10.2337/diacare.21.9.1414 · DOI
10.1161/hh2301.100342 · DOI
10.1016/S0092-8674(00)80701-1 · DOI
10.1073/pnas.012479199 · DOI
10.2337/db06-0732 · DOI
Kuo AL , Gulbis JM, Antcliff JF, Rahman T, Lowe ED, Zimmer J, Cuthbertson J, Ashcroft FM, Ezaki T, Doyle DA. Crystal structure of the potassium channel KirBac1. 1 in the closed state Science 300 : 1922–1926, 2003. · DOI
10.1074/jbc.271.18.10623 · DOI
10.1016/j.yjmcc.2005.03.009 · DOI
10.2337/db06-1275 · DOI
Matsuo M , Tanabe K, Kioka N, Amachi T, Ueda K. Different binding properties and affinities for ATP and ADP among sulfonylurea receptor subtypes, SUR1, SUR2A, and SUR2B. J Biol Chem 275 : 28757–28763, 2002. · DOI
10.1161/01.RES.87.10.873 · DOI
10.1038/sj.emboj.7600877 · DOI · Paper page
10.1016/j.yjmcc.2004.11.019 · DOI
10.1073/pnas.95.18.10402 · DOI
10.1073/pnas.94.22.11969 · DOI
10.2337/diab.46.11.1743 · DOI
10.1038/nature04711 · DOI
10.1126/science.272.5269.1785 · DOI
10.1016/S0092-8674(02)01227-8 · DOI
10.1038/305147a0 · DOI
10.1152/physrev.1987.67.4.1185 · DOI
10.1073/pnas.0404756101 · DOI
10.1093/hmg/ddl101 · DOI
10.1093/hmg/ddi305 · DOI
10.2337/db05-1420 · DOI
10.1038/sj.embor.7400393 · DOI
10.2337/diabetes.52.10.2630 · DOI
10.1016/0014-5793(95)01369-5 · DOI · Paper page
10.1074/jbc.275.13.9270 · DOI
10.1038/253635a0 · DOI
10.2337/diabetes.51.3.875 · DOI
10.1007/s11892-002-0071-9 · DOI
10.2337/db05-1640 · DOI
Shimomura K , Hörster F, de Wet H, Flanagan SE, Ellard S, Hattersley AT, Wolf NI, Ashcroft FM, Ebinger F. A novel mutation causing DEND syndrome—a treatable channelopathy of pancreas and brain. Neurology 2007 [Published on-line July 25, PMID 17652641]. · DOI
10.1126/science.282.5391.1138 · DOI · Paper page
10.1007/s00125-006-0407-0 · DOI
10.1038/sj.emboj.7600715 · DOI
10.1113/jphysiol.2005.099168 · DOI
10.2337/diabetes.53.suppl_3.S123 · DOI
10.2337/db06-0637 · DOI
10.1126/science.7716548 · DOI · Paper page
10.1007/BF00657506 · DOI
10.1038/387179a0 · DOI
10.1016/S0140-6736(98)07019-6 · DOI · Paper page
10.1016/S0896-6273(00)80708-4 · DOI · Paper page
10.1016/S0896-6273(01)00356-7 · DOI
10.1210/jc.2004-1241 · DOI

Sorted by citations

Items 101–102 of 102

DETERMINING KCNJ11 E23K POLYMORPHISM IN A GROUP OF VIETNAMESE POPULATION BY RESTRICTION FRAGMENT LENGTH POLYMORPHISM METHOD
Nguyễn, T. T. T., & Tran, B. Q. (2016) · doi:10.18173/2354-1059.2016-0071
“Glucose metabolism stimulates insulin secretion from pancreatic beta cells by closing KATP channels, thereby inducing beta cell depolarization, calcium influx, and insulin exocytosis [1] conversely, opening of KATP channels which prevents insulin secretion by causing beta cell hyper-polarization.”
Background
Cardiac ATP-Sensitive Potassium Channels and Associated Channelopathies
Alekseev, A., Reyes, S., Yamada, S., Park, S., Arrell, D., Kane, G. M., Olson, T. M., & Terzic, A. (2013) · Springer eBooks · doi:10.1007/978-1-4471-4881-4_15

Authors: Ashcroft, F. M.
Affiliations: University of Oxford (GB)
Corresponding author: Ashcroft, Frances M.
ORCID: Ashcroft, Frances M.
Venue: American Journal of Physiology-Endocrinology and Metabolism
Publisher: American Physiological Society
Published: 2007-10
Volume: 293
Issue: 4
Pages: E880-E889
ISSN: 0193-1849 (ISSN-L)
1522-1555
DOI: 10.1152/ajpendo.00348.2007
OpenAlex: W2134991186
Cited by: 107
References: 0
Citations by year: 2026: 3 · 2024: 1 · 2023: 3 · 2022: 1 · 2021: 6 · 2020: 7 · 2019: 1 · 2018: 2 · 2017: 8 · 2016: 10 · 2015: 1 · 2014: 6 · 2013: 10 · 2012: 6
FWCI: 12.29
Type: journal article
Language: en
Open access: closed
Locations: American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
PubMed (publishedVersion)
Funders: Wellcome Trust
Diabetes UK
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords: ATP-sensitive potassium channels, Kir6.2, SUR1, pancreatic beta cells, insulin secretion, glucose homeostasis, neonatal diabetes, congenital hyperinsulinism, ion channel mutations, channel structure and function
MeSH terms: Kcnj11 Channel, Adenosine Triphosphate, Animals, Diabetes Mellitus, Glucose, Homeostasis, Humans, Models, Biological, Models, Molecular, Mutation, Potassium Channels, Potassium Channels, Inwardly Rectifying, Channelopathies

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

ATP-sensitive K + channels and disease: from molecule to malady

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Citations

Cites

Cited by

Metadata

Record

About these checks