Congenital Hypothyroidism (Cretinism) in Neurod2-deficient Mice.
From: Clinical Research, Fred Hutchinson Cancer Research Center, Mailstop D4-100, 1100 Fairview Ave. N., Seattle, WA 98109, USA.
Molecular and cellular biology
- Publish Date: Jun 2006
- ISSN: 0270-7306
- Volume: 26
- Issue: 11
- Pages: 4311-5
- Medium: Print
- Language: English
- Citation (JAMA): Lin Chin-Hsing, Tapscott Stephen J, Olson James M, et al. Congenital Hypothyroidism (Cretinism) in Neurod2-deficient Mice.. Mol. Cell. Biol. Jun 2006;26:4311-5
Abstract
Mice lacking neuroD2, a basic helix-loop-helix transcription factor involved in brain development, show growth retardation and other abnormalities consistent with hypothalamic-pituitary-thyroid (HPT) axis dysfunction. neuroD2 is expressed in the paraventricular hypothalamic nuclei, the anterior lobe of pituitary, and the thyroid gland. In neuroD2-deficient mice, thyrotropin-releasing hormone, thyroid-stimulating hormone, and thyroid hormone are decreased in these three regions, respectively. neuroD2-null mice typically die 2 to 3 weeks after birth, but those treated with replacement doses of thyroxine survived more than 8 weeks. These data indicate that neuroD2 is expressed throughout the HPT axis and that all levels of the axis are functionally affected by its absence in mice.
Mesh Headings (Keywords): Animals, Basic Helix-Loop-Helix Transcription Factors, Congenital Hypothyroidism, Hypothalamus, Mice, Neuropeptides, Pituitary Gland, RNA, Messenger, Thyroid Gland
Check for Full Text / PubMed Unique Identifier (PMID): 16705180
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