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The thyroid hormone clearing type 3 deiodinase protects from cardiac congenital abnormalities

ABSTRACT: We examined the impact of thyroid hormone excess on the mouse fetal heart utilizing a model of deficiency in DIO3, the enzyme that is responsible for clearing thyroid hormones

ORGANISM(S): Mus musculus

PROVIDER: GSE198416 | GEO | 2022/11/23

REPOSITORIES: GEO

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The type 3 deiodinase contributes to the reduced sensitivity of the fetal brain to thyroid hormone

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Project description:Thyroid hormone receptor beta (THRB) is post-translationally modified by small ubiquitin-like modifier (SUMO). To investigate the biological role of THRB sumoylation, we generated a mouse model with a mutation that disrupts sumoylation at lysine 146 (K146Q). The THRB K146Q mutant mice had normal serum thyroxine (T4), markedly elevated serum thyrotropin (TSH) (81-fold above control), and enlargement of both the pituitary and the thyroid gland. The marked elevation in TSH, despite a normal serum T4 concentration, indicated blunted feedback regulation of TSH. TH profuction was 10-fold lower (per mg of thyroid tissue) in mutant mice compared to Wt mice.

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Thyroid hormone receptor alpha is required for thyroid hormone-dependent neural cell proliferation during tadpole metamorphosis

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