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Molecular and Cellular Biology, June 2006, p. 4311-4315, Vol. 26, No. 11
0270-7306/06/$08.00+0     doi:10.1128/MCB.02158-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Congenital Hypothyroidism (Cretinism) in neuroD2-Deficient Mice

Chin-Hsing Lin,1,2 Stephen J. Tapscott,2,3,4,6,7 and James M. Olson1,4,5,6,7*

Clinical Research,1 Human Biology Divisions, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, and Departments of,2 Neurology,3 Pathology,4 Pediatrics and Programs in,5 Neurobiology and Behavior,6 Molecular and Cellular Biology, University of Washington, Seattle, Washington 981057

Received 7 November 2005/ Returned for modification 9 December 2005/ Accepted 9 March 2006

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.

* Corresponding author. Mailing address: Fred Hutchinson Cancer Research Center, Mailstop D4-100, 1100 Fairview Ave. N., Seattle, WA 98109. Phone: (206) 667-7955. Fax: (206) 667-2917. E-mail: jolson{at}fhcrc.org.

Molecular and Cellular Biology, June 2006, p. 4311-4315, Vol. 26, No. 11
0270-7306/06/$08.00+0     doi:10.1128/MCB.02158-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.





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