{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTHRA encodes the thyroid hormone receptor α (TRα), a ligand‐activated transcription factor that exists as distinct isoforms due to alternative splicing—most notably, the T3‐binding TRα1 and the non–T3–binding variant TRα2. Detailed structural studies have revealed that TRα contains a flexible D‐domain capable of adopting different conformations, while precise posttranslational modifications such as acetylation modulate its DNA‐binding affinity and transcriptional activity. Moreover, crystallographic and mutagenesis analyses have uncovered additional ligand interaction surfaces and defined key single‐nucleotide polymorphisms within THRA that can influence receptor function and stability, thereby fine‐tuning the receptor’s ability to switch between coactivator and corepressor complexes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn vivo and clinical investigations have established that TRα plays a pivotal role in normal development, metabolism, and tissue differentiation. In patients and animal models harboring THRA mutations, defective TRα function manifests as growth retardation, skeletal dysplasia, and abnormal neurodevelopment—findings that underscore the receptor’s essential role in organ maturation and adipose as well as cardiac tissue homeostasis. Altered TRα expression has also been observed in adipose depots, where it appears to contribute to tissue expandability, while abnormal TRα signaling in neural progenitors leads to premature cell‐cycle exit and impaired cortical development. Such studies highlight the importance of an intact THRA gene in maintaining proper developmental and metabolic programs."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "21"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its developmental roles, aberrant THRA function has been implicated in various pathological settings. In thyroid and breast cancers, for example, altered TRα expression and mutation spectra contribute to abnormal gene regulation that may promote tumor progression and predict clinical outcome. Additionally, T3‐dependent regulation of downstream genes involved in matrix remodeling and cell proliferation (such as furin) implicates TRα in modulating invasiveness and oncogenic signaling. Emerging evidence further suggests that altered TRα activity under pathological conditions not only disrupts normal tissue repair—for example, in cardiac recovery—but also predisposes patients to hyperproliferative skin lesions, underscoring its potential as a therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "22", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Hege Berghagen, Erlend Ragnhildstveit, Kristin Krogsrud, et al. 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