{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSLC16A2, which encodes monocarboxylate transporter 8 (MCT8), is a highly specific, energy‐independent transmembrane protein that mediates the cellular uptake and efflux of iodothyronines—especially triiodothyronine (T3)—thereby regulating thyroid hormone (TH) bioavailability at the cellular level. Its discovery, through analyses of gene deletions and missense mutations associated with severe psychomotor retardation and abnormal TH serum profiles, established MCT8 as the principal TH transporter whose function is critical for proper neuronal signaling and development."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nExpression studies show that MCT8 is predominantly localized in neurons and is also found in other critical regions such as the blood–brain barrier, choroid plexus, and even oligodendrocytes. During brain development, MCT8 expression in these cell populations ensures efficient T3 delivery to key target cells, and its distribution in the cerebral microvasculature and in placental tissues supports its role in regulating both central and peripheral TH supply."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMutations in SLC16A2 are causative for disorders such as Allan–Herndon–Dudley syndrome, which is characterized by severe intellectual and motor impairments alongside atypical thyroid hormone profiles (with elevated free T3 and low or normal thyroxine and rT3 levels). Functional investigations in patient-derived cells and animal models have demonstrated that loss-of-function mutations impede T3 uptake into neurons, thereby disrupting intracellular T3 metabolism and signaling—a defect that underlies the profound neurodevelopmental deficits observed in these patients."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nDetailed molecular and structural analyses have provided additional insights into MCT8 function. Investigations indicate that MCT8 may operate as a monomer or homodimer and that specific amino acid residues—such as His192, which is sensitive to chemical modification—are critical for substrate recognition and transport activity. Moreover, a comparative evaluation with closely related transporters (for example, MCT10) underscores the unique specificity of MCT8 for iodothyronines, and studies in different cell types have revealed that subcellular trafficking and membrane localization of MCT8 can vary, potentially contributing to tissue‐specific differences in TH signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its central role in brain development, MCT8 is expressed in extraneural tissues such as the placenta, where its regulated expression is thought to modulate transplacental TH passage and ensure proper fetal growth—a process that may be altered in conditions like intrauterine growth restriction. Emerging evidence from studies on various physiological and pathophysiological models further highlights the broad significance of MCT8 in regulating TH homeostasis across tissues, with implications extending even to contexts such as cancer cell metabolism."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, the body of research on SLC16A2/MCT8 underscores its essential function as the gatekeeper for thyroid hormone entry into cells—a role that is indispensable for the maintenance of TH‐dependent gene regulation and neurodevelopment. Disruptions in MCT8 function, whether due to point mutations affecting transporter kinetics or perturbations in its cellular localization, lead to profound clinical syndromes characterized by neurocognitive deficits and altered peripheral TH metabolism.\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Edith C H Friesema, Annette Grueters, Heike Biebermann, et al. 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