PMID: 9183515Jan 1, 1996Paper

Biology of the congenitally hypothyroid hyt/hyt mouse

Advances in Neuroimmunology
E BiesiadaS A Stein

Abstract

The hyt/hyt mouse has an autosomal recessive, fetal onset, characterized by severe hypothyroidism that persists throughout life and is a reliable model of human sporadic congenital hypothyroidism. The hypothyroidism in the hyt/hyt mouse reflects the hyporesponsiveness of the thyroid gland to thyrotropin (TSH). This is attributable to a point mutation of C to T at nucleotide position 1666, resulting in the replacement of a Pro with Leu at position 556 in transmembrane domain IV of the G protein-linked TSH receptor. This mutation leads to a reduction in all cAMP-regulated events, including thyroid hormone synthesis. The diminution in T3/T4 in serum and other organs, including the brain, also leads to alterations in the level and timing of expression of critical brain molecules, i.e. selected tubulin isoforms (M beta 5, M beta 2, and M alpha 1), microtubule associated proteins (MAPs), and myelin basic protein, as well as to changes in important neuronal cytoskeletal events, i.e. microtubule assembly and SCa and SCb axonal transport. In the hyt/hyt mouse, fetal hypothyroidism leads to reductions in M beta 5, M beta 2, and M alpha 1 mRNAs, important tubulin isoforms, and M beta 5 and M beta 2 proteins, which comprise the microtubule...Continue Reading

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Citations

Jan 9, 2009·The Cerebellum·Noriyuki Koibuchi
Jan 8, 1999·Brain Research. Developmental Brain Research·S GianinoX M Xu
Sep 1, 2005·Thyroid : Official Journal of the American Thyroid Association·Valerie Anne Galton
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Jan 18, 2021·Immunology·Martin JaegerRomana T Netea-Maier
Aug 12, 2009·Progress in Neurobiology·Carolina Estima FlemingMónica Mendes Sousa

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