Deiodinase Type 3
Mostrando 1-12 de 33 artigos, teses e dissertações.
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1. Propranolol inhibits myocardial infarction-induced brown adipose tissue D2 activation and maintains a low thyroid hormone state in rats
Considering the recognized role of thyroid hormones on the cardiovascular system during health and disease, we hypothesized that type 2 deiodinase (D2) activity, the main activation pathway of thyroxine (T4)-to-triiodothyronine (T3), could be an important site to modulate thyroid hormone status, which would then constitute a possible target for β-adrenergic
Braz J Med Biol Res. Publicado em: 10/10/2019
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2. Os hormônios tireoideanos e o desenvolvimento esquelético fetal e pós-natal: estudo do padrão de expressão dos transportadores e das selenodesiodases das iodotironinas. / Thyroid hormone and skeletal development at fetal and postnatal ages: the expression pattern of iodothyronine transporters and deiodinases.
Thyroid hormone (TH) plays a key role on post-natal bone development and metabolism, while its relevance during fetal bone development is uncertain. To study this, pregnant mice and fetuses were made hypothyroid. The skeleton morphology was preserved up to 16.5 embryonic days (E). Only at E18.5, the hypothyroid fetuses exhibited a reduction in femoral type I
Publicado em: 2009
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3. A thyroid hormone-regulated gene in Xenopus laevis encodes a type III iodothyronine 5-deiodinase.
The type III iodothyronine 5-deiodinase metabolizes thyroxine and 3,5,3'-triiodothyronine to inactive metabolites by catalyzing the removal of iodine from the inner ring. The enzyme is expressed in a tissue-specific pattern during particular stages of development in amphibia, birds, and mammals. Recently, a PCR-based subtractive hybridization technique has b
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4. Metamorphosis is inhibited in transgenic Xenopus laevis tadpoles that overexpress type III deiodinase
One of the genes that is up-regulated by thyroid hormone (TH) during Xenopus laevis metamorphosis encodes a type III deiodinase (D3) that inactivates TH. Transgenic X. laevis tadpoles overexpressing a GFP-D3 fusion protein were produced. These transgenic tadpoles had high levels of deiodinase activity and were resistant to exogenous TH added 1 week after fer
The National Academy of Sciences.
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5. Kinetic evidence suggesting two mechanisms for iodothyronine 5'-deiodination in rat cerebral cortex.
Enzymatic 5'-deiodination of 3,3',5'-triiodothyronine (rT3) and 3,3',5,5'-tetraiodothyronine (thyroxine, T4) was studied in microsomal preparations of rat cerebral cortex. Evidence was obtained for the existence of two thiol-dependent 5'-deiodinase entities. One of these predominates in tissue from euthyroid and long-term hypothyroid rats, is specific for rT
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6. Type 2 iodothyronine deiodinase is highly expressed in human thyroid.
Type 2 iodothyronine deiodinase (D2) is a recently cloned selenodeiodinase thought to provide intracellular 3,5,3' triiodothyronine (T3) to a restricted group of tissues. We report here the presence of D2 mRNA in human thyroid at levels 50-150-fold higher than in placenta. Surprisingly, while type 1 deiodinase (D1) is known to be present in human thyroid, D2
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7. Type 3 lodothyronine deiodinase: cloning, in vitro expression, and functional analysis of the placental selenoenzyme.
Type 3 iodothyronine deiodinase (D3) catalyzes the conversion of T4 and T3 to inactive metabolites. It is highly expressed in placenta and thus can regulate circulating fetal thyroid hormone concentrations throughout gestation. We have cloned and expressed a 2.1-kb human placental D3 cDNA which encodes a 32-kD protein with a Km of 1.2 nM for 5 deiodination o
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8. Potential of brown adipose tissue type II thyroxine 5'-deiodinase as a local and systemic source of triiodothyronine in rats.
Previous reports suggest that a type II iodothyronine 5'-deiodinase may become the main enzymatic pathway for extrathyroidal triiodothyronine (T3) generation when the enzyme levels are sufficiently elevated and/or liver and kidney type I 5'-deiodinase activity is depressed. The present studies assessed the potential of brown adipose tissue (BAT) type II 5'-d
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9. Knockdown of the Type 3 Iodothyronine Deiodinase (D3) Interacting Protein Peroxiredoxin 3 Decreases D3-Mediated Deiodination in Intact Cells
The type 3 iodothyronine deiodinase (D3) is the primary deiodinase that inactivates thyroid hormone. Immunoprecipitation of D3, followed by fluorescent two-dimensional difference gel electrophoresis and mass spectrometry, identified peroxiredoxin 3 (Prx3) as a D3-associated protein. This interaction was confirmed using reverse coimmunoprecipitation, in which
The Endocrine Society.
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10. The type 2 iodothyronine deiodinase is expressed primarily in glial cells in the neonatal rat brain
Thyroid hormone plays an essential role in mammalian brain maturation and function, in large part by regulating the expression of specific neuronal genes. In this tissue, the type 2 deiodinase (D2) appears to be essential for providing adequate levels of the active thyroid hormone 3,5,3′-triiodothyronine (T3) during the developmental period. We have studie
The National Academy of Sciences of the USA.
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11. Pregnant rat uterus expresses high levels of the type 3 iodothyronine deiodinase
Although thyroid hormones are critically important for the coordination of morphogenic processes in the fetus and neonate, premature exposure of the embryo to levels of the hormones present in the adult is detrimental and can result in growth retardation, malformations, and even death. We report here that the pregnant rat uterus expresses extremely high leve
American Society for Clinical Investigation.
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12. Hearing loss and retarded cochlear development in mice lacking type 2 iodothyronine deiodinase
The later stages of cochlear differentiation and the developmental onset of hearing require thyroid hormone. Although thyroid hormone receptors (TRs) are a prerequisite for this process, it is likely that other factors modify TR activity during cochlear development. The mouse cochlea expresses type 2 deiodinase (D2), an enzyme that converts thyroxine, the ma
National Academy of Sciences.