2.A.1.13.3
The thyroid hormone transporter, MCT8 (transports L- and D-isomers of thyroxine (T4), 3,3',5-triiodothyronine (T3), 3,3'5'-triiodothyronine (rT3) and 3,3'-diiodothyronine [Km values = 2-5 μM; Leu, Phe, Trp and Tyr were not transported]) (Friesema et al., 2003). Loss of function mutations in MCT8 leads to Allan-Herndon-Dudley syndrome, severe X-linked psychomotor retardation and elevated serum T3 levels (Jansen et al., 2008). Essential molecular determinants for thyroid hormone transport and their structural implications are presented by Kinne et al. (2010). Induced by retinoic acid (Kogai et al., 2010). Mediates energy-independent bidirectional transport. MCT8 is specific for L-iodothyronines and requires at least one iodine atom per aromatic ring. Thyronamines, decarboxylated metabolites of iodothyronines, triiodothyroacetic acid and tetraiodothyroacetic acid, TH derivatives lacking both chiral center and amino group, are not substrates (Kinne et al., 2010). A deficiency causes altered thyroid morphology and a persistent high triiodothyronine/thyroxine ratio after thyroidectomy (Wirth et al., 2011). Primary and secondary thyroid hormone transporters have been reviewed (Kinne et al., 2011). A differential effect of a shortage of thyroid hormone was observed compared with a knockout of thyroid hormone transporters Mct8 and Mct10 on murine macrophage polarization (Hoen et al. 2024).