The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
KIR6.2 Polymorphism Predisposes to Type 2 Diabetes by Inducing Overactivity of Pancreatic β-Cell ATP-Sensitive K+ Channels
Abstract
E23K, a common single nucleotide polymorphism in KIR6.2, the pore-forming subunit of pancreatic β-cell ATP-sensitive K+ channels, significantly enhanced open probability of these channels, thus reducing their sensitivity toward inhibitory ATP4− and increasing the threshold concentration for insulin release. Previous association studies and high allelic frequency suggest this effect to critically inhibit secretion and play a major role in pathogenesis of common type 2 diabetes. Based on evidence for functional relevance of E23K in both the heterozygous (E/K; with E in position 23 of KIR6.2 in one allele and K in the other) and homozygous (K/K; with K in position 23 of KIR6.2 in both alleles) genotype, we propose a model in which enhanced susceptibility to type 2 diabetes is associated with evolutionary advantage of the E/K state.
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Citations
Cites
Sakura, H., Wat, N., Horton, V., Millns, H., Turner, R. C., & Ashcroft, F. M. (1996) · Diabetologia · doi:10.1007/bf02658512 · Cited by 122
Markworth, E., Schwanstecher, C., & Schwanstecher, M. (2000) · Diabetes · doi:10.2337/diabetes.49.9.1413 · Cited by 76
Self-citation
Cited by
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
KATP channels as molecular sensors of cellular metabolism
Nichols, C. G. (2006) · Nature · doi:10.1038/nature04711 · Cited by 851
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
ATP-sensitive potassium channelopathies: focus on insulin secretion
Ashcroft, F. M. (2005) · Journal of Clinical Investigation · doi:10.1172/jci25495 · Cited by 623
Physiology of Proglucagon Peptides: Role of Glucagon and GLP-1 in Health and Disease
Sandoval, D. A., & D'Alessio, D. A. (2015) · Physiological Reviews · doi:10.1152/physrev.00013.2014 · Cited by 498
Metadata
- Authors
- Schwanstecher, C., Meyer, U., & Schwanstecher, M.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2002-03-01
- Volume
- 51
- Issue
- 3
- Pages
- 875-879
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2086605260
- Cited by
- 243
- References
- 2
- FWCI
- 17.54
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: KIR6.2 Polymorphism Predisposes to Type 2 Diabetes by Inducing Overactivity of Pancreatic β-Cell ATP-Sensitive K+ Channels. https://app.cochat.ai/papers/10.2337/diabetes.51.3.875
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- Schwanstecher, C., Meyer, U., & Schwanstecher, M. (2002). KIR6.2 Polymorphism Predisposes to Type 2 Diabetes by Inducing Overactivity of Pancreatic β-Cell ATP-Sensitive K+ Channels. Diabetes. https://doi.org/10.2337/diabetes.51.3.875
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
