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Journal Article

Congenital hypothyroid Pax8(-/-) mutant mice can be rescued by inactivating the TR alpha gene

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Mansouri,  A.
Research Group of Molecular Cell Differentiation, MPI for biophysical chemistry, Max Planck Society;

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Citation

Flamant, F., Poguet, A. L., Plateroti, M., Chassande, O., Gauthier, K., Streichenberger, N., et al. (2002). Congenital hypothyroid Pax8(-/-) mutant mice can be rescued by inactivating the TR alpha gene. Molecular Endocrinology, 16(1), 24-32. Retrieved from http://mend.endojournals.org/cgi/reprint/16/1/24.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0012-F47C-1
Abstract
Mice devoid of all TRs are viable, whereas Pax8(-/-)mice, which lack the follicular cells producing T-4 and T-3 in the thyroid gland, die during the first weeks of postnatal life. A precise comparison between the two types of mutants reveals that their phenotypes are similar, but the defects in spleen, bone, and small intestine are more pronounced in Pax(-/-) mice. This is interpreted as the result of a negative effect of the unliganded TR on thyroid hormone target genes expression in the Pax(-/-)mutants. Pax8(-/-) compound mutants can survive to adulthood, and the expression of target genes is partially restored. This demonstrates the importance of TR alpha aporeceptor activity in several aspects of postnatal development.