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S Benvenuti, P Luciani, I Cellai, C Deledda, S Baglioni, R Saccardi, S Urbani, F Francini, R Squecco, C Giuliani, G B Vannelli, M Serio, A Pinchera and A Peri

-regulated activity of type II and III iodothyronine deiodinases (D2 and 3) in different brain areas is essential during brain development ( Kester et al . 2004 ). Accordingly, it has been shown that early maternal hypothyroxinemia alters fetal brain histogenesis and

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Shiao Y Chan, Laura A Hancox, Azucena Martín-Santos, Laurence S Loubière, Merlin N M Walter, Ana-Maria González, Phillip M Cox, Ann Logan, Christopher J McCabe, Jayne A Franklyn and Mark D Kilby

-restricted fetal guinea pigs has shown a compensatory increase in brain deiodinase type 2 (DIO2) expression, which could increase local concentrations of the active thyroid hormone (TH) ligand, T 3 , from T 4 conversion ( Chan et al . 2005 ). In clinical practice

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Anna de Lloyd, James Bursell, John W Gregory, D Aled Rees and Marian Ludgate

) , applied several transcript detection and biochemical techniques to provide evidence of functional TSHRs in human osteoblast-like (hOB) cells. Morimura et al . (2005) studied the expression of functional TSHR and type 2 iodothyronine deiodinase (D2) in

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Jonathan J Nicholls, Mary Jane Brassill, Graham R Williams and J H Duncan Bassett

inactivates T 3 , resulting in the repression of T 3 -target gene transcription. PVN, paraventricular nucleus; TRH, thyrotrophin-releasing hormone; TSH, thyroid-stimulating hormone; DIO1, DIO2 and DIO3, type 1, 2 and 3 deiodinases; MCT8 and MCT10

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F Aréchiga-Ceballos, E Alvarez-Salas, G Matamoros-Trejo, M I Amaya, C García-Luna and P de Gortari

activates type 2 deiodinase (D2) enzymatic activity in the median eminence ( Coppola et al . 2005 a ), which in turn increases local T 3 content in the hypothalamus, inhibiting proTRH expression. In contrast, hyperphagia and being overweight lead to high

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Lars P Klieverik, Ewout Foppen, Mariëtte T Ackermans, Mireille J Serlie, Hans P Sauerwein, Thomas S Scanlan, David K Grandy, Eric Fliers and Andries Kalsbeek

removal of the carboxylate group on the β-alanine side chain in addition to deiodination. Indeed, thyronamines have recently been identified as isoenzyme-specific substrates of the iodothyronine deiodinases type 1, 2, and 3 ( Piehl et al . 2008 ). T 1 AM

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Hsiu-Chi Lee and Shaw-Jenq Tsai

secreted by thyroid gland is the prohormone, thyroxine (T4). Once in the target tissue, T4 can be converted to 3,5,3′-triiodothyronine (T3, active form) or reverse T3 (rT3, inactive form). This action is modulated by different iodothyronine deiodinases. The

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Joke Delbaere, Pieter Vancamp, Stijn L J Van Herck, Nele M A Bourgeois, Mary J Green, Richard J T Wingate and Veerle M Darras

regulated by deiodinases and transmembrane transporters ( Bianco & Kim 2006 , Visser et al . 2008 ). In recent years, there has been a growing awareness of the requirement for monocarboxylate transporter 8 (MCT8) in neurodevelopment, through its role in

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M T Ackermans, L P Klieverik, P Ringeling, E Endert, A Kalsbeek and E Fliers

the human deiodinases. The decarboxylating enzyme, however, still remains to be identified. Pyridoxal-5-phosphate-dependent aromatic L-amino acid decarboxylase (AADC) is a promising candidate, although Hoefig et al . (2009) recently reported that

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Sandra Ghelardoni, Grazia Chiellini, Sabina Frascarelli, Alessandro Saba and Riccardo Zucchi

on the order of 70%. Most of the balance was accounted for by oxidative deamination, yielding the thyroacetic derivative TA1 that was detectable in cell lysate and medium within a few minutes. Although D1 deiodinase has been reported to be expressed