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of the thyroid follicular cell, is a potent suppressor of thyroid-specific gene expression, and that this action of Tg overcomes TSH-mediated effects. Thus, it appears that Tg is a feedback suppressor of its own expression, as well as of TPO, NIS and
Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA
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Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA
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Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA
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Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA
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Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA
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Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA
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Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Pungnap-dong, Songpa-gu, Seoul 138-736, South Korea
The Howard Hughes Medical Institute and
The Department of Hematology, University of Washington, Seattle, Washington 98195, USA
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), sodium iodide symporter, and the thyroid-stimulating hormone receptor (TSHR) genes, all of which are under the regulatory control of TSH and insulin/insulin-like growth factor-I (IGF-I). Moreover, the growth of FRTL-5 cells is regulated by several
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even more dramatic surge of plasma 3,5,3′-tri-iodothyronine (T 3 ). The underlying cause of augmented TH secretion shortly before hatching is unknown. Some authors have speculated that elevated thyroidal and pituitary sensitivity to thyrotrophin (TSH
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, and liver. Thyrotropin (TSH), T 3 , and T 4 serum concentrations TSH was measured by specific RIA, using a kit for rat TSH supplied by the NIDDKD (NIH) and data were expressed in terms of the reference preparation provided (RP-3). The intra
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Introduction Thyroid hormones are involved in the regulation of growth, metabolism, heat production, gonadal development, molting, migration, and hatching in birds ( McNabb 2000 ). Thyroid-stimulating hormone (TSH) plays an important
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understanding regarding the degree of hypothyroidism previously reported in EO animal models. Because circulating thyrotropin (TSH) was unaltered in adult small litter (SL) rats, we evaluated the thyrotropin release hormone (TRH) in the hypothalamus, the TSH in
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ascertained ( Donda et al. 1990 ). Cheron et al. (1980) reported lower serum T3 and higher serum thyroid-stimulating hormone (TSH) in adults than in 21- and 30-day-old pre-pubertal male (Pm) rats, without any significant difference in serum T4
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TSH concentration in rats, potentially due to leptin action at the hypothalamus, as the direct pituitary effect of leptin on TSH release was inhibitory, potentially as a result of an autocrine–paracrine effect exerted by locally produced leptin
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in intact rats reported that TSH administration increases rat tDh (rtDh) activity ( Roche et al . 1953 , Maayan & Rosenberg 1963 ). Similarly, thyroidal ID1 activity ( Erickson et al . 1982 ) and mRNA ( Toyoda et al . 1992 ) are increased by TSH
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β sub-units of thyroid-stimulating hormone (TSH). These cells lack receptors for the hypothalamic thyrotropin-releasing hormone (TRH) ( Bockmann et al . 1997 ), and do not respond to conventional hypothalamic outputs. In mammals, the MT1 receptor co