Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes.

By A. Gloyn, E. Pearson, Jennifer F. Antcliff, P. Proks, G. Bruining, A. S. Slingerland, Neville J. Howard, S. Srinivasan, Jose Silva, J. Molnes and 15 more. New England Journal of Medicine, 2004

1,162 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Pathology and Forensic Medicine, Surgery

View Paper: https://www.semanticscholar.org/paper/e13ad19c7f931d8c9c502b00ca4623203c06bbeb

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

1. A. Kashiwagi
2. M. Kasuga
3. E. Araki
4. T. Hanafusa
5. K. Ueki
6. Takashi Kadowaki
7. Kazuharu Furutani
8. Y. Iwamoto

Citations in the corpus

• Inwardly rectifying potassium channels: their structure, function, and physiological roles. (2010, background): “2, which cause neonatal diabetes alone, directly impair ATP binding (16, 210, 211, 344, 629).”
• Report of the Committee on the Classification and Diagnostic Criteria of Diabetes Mellitus (2010, background): “2 and SUR1, which form the KATP channel in pancreatic b-cells, have been identified [31, 32].”