Diabetic Risk Factors Promote Islet Amyloid Polypeptide Misfolding by a Common, Membrane-mediated Mechanism
Author:
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/srep31094.pdf
Reference48 articles.
1. Butler, A. E. et al. Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes. Diabetes 52, 102–110 (2003).
2. Hull, R. L., Westermark, G. T., Westermark, P. & Kahn, S. E. Islet amyloid: a critical entity in the pathogenesis of type 2 diabetes. J. Clin. Endocrinol. Metab. 89, 3629–3643 (2004).
3. Ashcroft, F. M. & Rorsman, P. Diabetes Mellitus and the β Cell: The Last Ten Years. Cell 148, 1160–1171 (2012).
4. Haataja, L., Gurlo, T., Huang, C. J. & Butler, P. C. Islet amyloid in type 2 diabetes and the toxic oligomer hypothesis. Endocr. Rev. 29, 303–316 (2008).
5. Rustenbeck, I., Matthies, A. & Lenzen, S. Lipid composition of glucose-stimulated pancreatic islets and insulin-secreting tumor cells. Lipids 29, 685–692 (1994).
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