The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Abnormalities of pancreatic islets by targeted expression of a dominant-negative K ATP channel
Open accessAbstract
ATP-sensitive K + (K ATP ) channels are known to play important roles in various cellular functions, but the direct consequences of disruption of K ATP channel function are largely unknown. We have generated transgenic mice expressing a dominant-negative form of the K ATP 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. K ATP 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 K ATP channel might play a significant role in beta cell survival in addition to its role in the regulation of insulin secretion.
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Cites
Glucose induces closure of single potassium channels in isolated rat pancreatic β-cells
Ashcroft, F. M., Harrison, D. E., & Ashcroft, S. J. H. (1984) · Nature · doi:10.1038/312446a0 · Cited by 1,113
Thomas, P. M., Cote, G. J., Wohllk, N., Haddad, B., Mathew, P. M., Rabl, W., Aguilar-Bryan, L., Gagel, R. F., & Bryan, J. (1995) · Science · doi:10.1126/science.7716548 · Cited by 806
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
Cited by
Triggering and amplifying pathways of regulation of insulin secretion by glucose.
Henquin, J. C. (2000) · Diabetes · doi:10.2337/diabetes.49.11.1751 · Cited by 1,201
Molecular Biology of Adenosine Triphosphate-Sensitive Potassium Channels*
Aguilar-Bryan, L., & Bryan, J. (1999) · Endocrine Reviews · doi:10.1210/edrv.20.2.0361 · Cited by 698
Defective insulin secretion and enhanced insulin action in K ATP channel-deficient mice
Miki, T., Nagashima, K., Tashiro, F., Kotake, K., Yoshitomi, H., Tamamoto, A., Gonoi, T., Iwanaga, T., Miyazaki, J.-I., & Seino, S. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.18.10402 · Cited by 502
Self-citationActivating Mutations in Kir6.2 and Neonatal Diabetes
Hattersley, A. T., & Ashcroft, F. M. (2005) · Diabetes · doi:10.2337/diabetes.54.9.2503 · Cited by 414
Hyperinsulinism in Infancy: From Basic Science to Clinical Disease
DUNNE, M. J., COSGROVE, K. E., SHEPHERD, R. M., AYNSLEY-GREEN, A., & LINDLEY, K. J. (2004) · Physiological Reviews · doi:10.1152/physrev.00022.2003 · Cited by 294
Metadata
- Authors
- Miki, T., Tashiro, F., Iwanaga, T., Nagashima, K., Yoshitomi, H., Aihara, H., Nitta, Y., Gonoi, T., Inagaki, N., Miyazaki, J.-I., & Seino, S.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1997-10-28
- Volume
- 94
- Issue
- 22
- Pages
- 11969-11973
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2034158559
- Cited by
- 180
- References
- 3
- FWCI
- 15.28
- Type
- journal article
- Language
- en
- Open access
- green
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- Miki, T., Tashiro, F., Iwanaga, T., Nagashima, K., Yoshitomi, H., Aihara, H., Nitta, Y., Gonoi, T., Inagaki, N., Miyazaki, J.-I., & Seino, S. (1997). Abnormalities of pancreatic islets by targeted expression of a dominant-negative K ATP channel. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.94.22.11969
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