Sites: The local veterinarian (RD) contributed clinical assessment, sample collection, and contacts with participating breeders. Enzymology, histopathology, and molecular investigations were performed at the College of Veterinary Medicine, Michigan State University, East Lansing, MI.
Congenital Hypothyroidism with Goiter in Tenterfield Terriers
Version of Record online: 1 NOV 2012
Copyright © 2012 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 26, Issue 6, pages 1350–1357, November/December 2012
How to Cite
Dodgson, S.E., Day, R. and Fyfe, J.C. (2012), Congenital Hypothyroidism with Goiter in Tenterfield Terriers. Journal of Veterinary Internal Medicine, 26: 1350–1357. doi: 10.1111/j.1939-1676.2012.01015.x
Meeting presentation: These data were presented as a poster in preliminary form at the 5th International Conference: Advances in Canine and Feline Genomics and Inherited Diseases, Baltimore, MD, September 22–25, 2010
- Issue online: 20 NOV 2012
- Version of Record online: 1 NOV 2012
- Manuscript Accepted: 5 SEP 2012
- Manuscript Revised: 15 AUG 2012
- Manuscript Received: 20 APR 2012
- Peabody Award
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|jvim1015-sup-0001-FigureS1.tif||image/tif||5889K||Figure S1. Photomicrograph of thyroid tissue from a 5-week-old Tenterfield Terrier exhibiting CHG. There is diffuse follicular epithelial cell hyperplasia. Follicle spaces are largely obliterated by cuboidal to columnar epithelial cells piled up as blunt papillae and exhibiting multiple small cytoplasmic vacuoles. The remaining colloid spaces are small and have scant, poorly staining colloid. The bar indicates 200 μm.|
|jvim1015-sup-0002-FigureS2.tif||image/tif||19540K||Figure S2. Local structure modeling demonstrating the predicted effect of the Tenterfield Terrier mutation in TPO. The structure of human myeloperoxidase, a TPO homologue, determined from high-resolution x-ray crystallographic data is illustrated herein as a discontinuous ribbon diagram using the PyMOL Molecular Graphics System. A star denotes the residue homologous to R593 which is replaced by tryptophan in CHG-affected dogs. The hydrogen bonds formed between the residues homologous to R593, aspartate 642, and tyrosine 637 in canine TPO are shown as dashed lines. Disruption of this hydrogen bonding sequence likely interferes with the maintenance of local protein structure necessary for arginine 591 to coordinate the heme group (in red), a key interaction required for TPO catalytic activity.|
Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.