| First Author | Lin CH | Year | 2006 |
| Journal | Mol Cell Biol | Volume | 26 |
| Issue | 11 | Pages | 4311-5 |
| PubMed ID | 16705180 | Mgi Jnum | J:109615 |
| Mgi Id | MGI:3629365 | Doi | 10.1128/MCB.02158-05 |
| Citation | Lin CH, et al. (2006) Congenital hypothyroidism (cretinism) in neuroD2-deficient mice. Mol Cell Biol 26(11):4311-5 |
| abstractText | 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. |
