Congenital Hypothyroid Pax8−/− Mutant Mice Can Be Rescued by Inactivating the TRα Gene | Zendy

Frédéric Flamant | Zendy; Anne-Lise Poguet | Zendy; Michelina Plateroti | Zendy; Olivier Chassande | Zendy; Karine Gauthier | Zendy; Nathalie Streichenberger | Zendy; Ahmed Mansouri | Zendy; Jacques Samarut | Zendy

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Congenital Hypothyroid Pax8−/− Mutant Mice Can Be Rescued by Inactivating the TRα Gene

Author(s) -

Frédéric Flamant,

Anne-Lise Poguet,

Michelina Plateroti,

Olivier Chassande,

Karine Gauthier,

Nathalie Streichenberger,

Ahmed Mansouri,

Jacques Samarut

Publication year - 2002

Publication title -

molecular endocrinology

Language(s) - English

Resource type - Journals

eISSN - 1944-9917

pISSN - 0888-8809

DOI - 10.1210/mend.16.1.0766

Subject(s) - pax8 , biology , mutant , thyroid , phenotype , gene , microbiology and biotechnology , medicine , spleen , endocrinology , transcription factor , genetics , immunology

Mice devoid of all TRs are viable, whereas Pax8(-/-) mice, which lack the follicular cells producing T4 and T3 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 Pax8(-/-) mice. This is interpreted as the result of a negative effect of the unliganded TR on thyroid hormone target genes expression in the Pax8(-/-) mutants. Pax8/TRalpha compound mutants can survive to adulthood, and the expression of target genes is partially restored. This demonstrates the importance of TRalpha aporeceptor activity in several aspects of postnatal development.

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