- About this Journal
- Abstracting and Indexing
- Aims and Scope
- Annual Issues
- Article Processing Charges
- Articles in Press
- Author Guidelines
- Bibliographic Information
- Citations to this Journal
- Contact Information
- Editorial Board
- Editorial Workflow
- Free eTOC Alerts
- Publication Ethics
- Reviewers Acknowledgment
- Submit a Manuscript
- Subscription Information
- Table of Contents
Clinical and Developmental Immunology
Volume 2012 (2012), Article ID 340542, 5 pages
Thr92Ala Polymorphism of Human Type 2 Deiodinase Gene (hD2) Affects the Development of Graves' Disease, Treatment Efficiency, and Rate of Remission
1Institute of Endocrinology, Almazov Federal Heart, Blood and Endocrinology Centre, 2 Akkuratova Street, Saint-Petersburg 197541, Russia
2Institute of Molecular Biology and Genetics, Almazov Federal Heart, Blood and Endocrinology Centre, 2 Akkuratova Street, Saint-Petersburg 197541, Russia
3Department of Mathematical Modeling, Almazov Federal Heart, Blood and Endocrinology Centre, 2 Akkuratova street, Saint-Petersburg 197541, Russia
Received 14 June 2012; Revised 7 October 2012; Accepted 18 October 2012
Academic Editor: Shervin Assassi
Copyright © 2012 Babenko Alina et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
- Z. Schroner, M. Javorsky, M. Kozarova, and I. Tkac, “Pharmacogenetics of oral antidiabetic treatment,” Bratislavské Lekárske Listy, vol. 112, no. 8, pp. 441–446, 2011.
- A. C. Bianco, D. Salvatore, B. Gereben, M. J. Berry, and P. R. Larsen, “Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases,” Endocrine Reviews, vol. 23, no. 1, pp. 38–89, 2002.
- J. Köhrle, “Local activation and inactivation of thyroid hormones: the deiodinase family,” Molecular and Cellular Endocrinology, vol. 151, no. 1-2, pp. 103–119, 1999.
- D. Salvatore, T. Bartha, J. W. Harney, and P. R. Larsen, “Molecular biological and biochemical characterization of the human type 2 selenodeiodinase,” Endocrinology, vol. 137, no. 8, pp. 3308–3315, 1996.
- R. P. Peeters, H. Van Toor, W. Klootwijk et al., “Polymorphisms in thyroid hormone pathway genes are associated with plasma TSH and iodothyronine levels in healthy subjects,” Journal of Clinical Endocrinology and Metabolism, vol. 88, no. 6, pp. 2880–2888, 2003.
- R. P. Peeters, W. M. van der Deure, and T. J. Visser, “Genetic variation in thyroid hormone pathway genes; polymorphisms in the TSH receptor and the iodothyronine deiodinases,” European Journal of Endocrinology, vol. 155, no. 5, pp. 655–662, 2006.
- A. L. Maia, B. W. Kim, S. A. Huang, J. W. Harney, and P. R. Larsen, “Type 2 iodothyronine deiodinase is the major source of plasma T3 in euthyroid humans,” The Journal of Clinical Investigation, vol. 115, no. 9, pp. 2524–2533, 2005.
- J. T. Nicoloff, S. M. Lum, C. A. Spencer, and R. Morris, “Peripheral autoregulation of thyroxine to triiodothyronine conversion in man,” Hormone and Metabolic Research, Supplement, vol. 14, pp. 74–79, 1984.
- A. Pilo, G. Iervasi, F. Vitek, M. Ferdeghini, F. Cazzuola, and R. Bianchi, “Thyroidal and peripheral production of 3,5,3'-triiodothyronine in humans by multicompartmental analysis,” American Journal of Physiology, vol. 258, no. 4, pp. E715–E726, 1990.
- D. Salvatore, H. Tu, J. W. Harney, and P. R. Larsen, “Type 2 iodothyronine deiodinase is highly expressed in human thyroid,” The Journal of Clinical Investigation, vol. 98, no. 4, pp. 962–968, 1996.
- J. Pachucki, J. Hopkins, R. Peeters et al., “Type 2 iodothyronine deiodinase transgene expression in the mouse heart causes cardiac-specific thyrotoxicosis,” Endocrinology, vol. 142, no. 1, pp. 13–20, 2001.
- L. H. Canani, C. Capp, J. M. Dora et al., “The type 2 deiodinase A/G (Thr92Ala) polymorphism is associated with decreased enzyme velocity and increased insulin resistance in patients with type 2 diabetes mellitus,” Journal of Clinical Endocrinology and Metabolism, vol. 90, no. 6, pp. 3472–3478, 2005.
- T. W. Guo, F. C. Zhang, M. S. Yang et al., “Positive association of the DIO2 (deiodinase type 2) gene with mental retardation in the iodine-deficient areas of China,” Journal of Medical Genetics, vol. 41, no. 8, pp. 585–590, 2004.
- D. Mentuccia, L. Proietti-Pannunzi, K. Tanner et al., “Association between a novel variant of the human type 2 deiodinase gene Thr92Ala and insulin resistance: evidence of interaction with the Trp64Arg variant of the beta-3-adrenergic receptor,” Diabetes, vol. 51, no. 3, pp. 880–883, 2002.
- O. Gumieniak, T. S. Perlstein, J. S. Williams et al., “Ala92 type 2 deiodinase allele increases risk for the development of hypertension,” Hypertension, vol. 49, no. 3, pp. 461–466, 2007.
- E. Grineva, A. Babenko, N. Vahrameeva et al., “Type 2 deiodinase Thr92Ala polymorphism impact on clinical course and myocardial remodeling in patients with graves' disease,” Cell Cycle, vol. 8, no. 16, pp. 2565–2569, 2009.
- R. S. Bahn, H. B. Burch, D. S. Cooper, et al., “Hyperthyroidism management guidelines,” Endocrine Practice, vol. 17, no. 3, pp. 1–65, 2011.