{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThyroid stimulating hormone β (TSHB) encodes the unique β‐subunit of thyroid stimulating hormone, which dimerizes with a common α‐subunit to generate a hormone essential for pituitary regulation of thyroid function. In its canonical role, TSH (via TSHB) binds to the TSH receptor on thyroid follicular cells to stimulate thyroid hormone synthesis, thereby maintaining metabolic homeostasis, growth, and development. Transcriptional regulation by pituitary‐restricted factors (such as Pit‐1 and cooperating nuclear receptors) ensures proper TSHB expression, and mutations or splice defects in TSHB are directly linked to congenital central hypothyroidism with consequent disruptions in thyroid hormone output, altered thyrocyte proliferation, and even adverse pregnancy outcomes and longevity shifts."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEmerging evidence extends the role of TSHB beyond traditional endocrine regulation. Alternative splice variants and peripheral expression of TSHB have been detected in immune cells, thyroid tissue, and even in adipose and bone‐marrow compartments—suggesting paracrine and autocrine actions that modulate local immune responses, osteoblastogenesis, cholesterol metabolism, and potentially even reproductive biology. In parallel, common genetic variants and epistatic interactions in the TSHB gene associate with risks for premature ovarian failure and, in some contexts, altered oncogenic potential in thyroid and breast tissues. Functional dissection of specific TSHB mutations has revealed that while some variants diminish cyclic adenosine monophosphate (cAMP) signaling, alternate pathways such as mitogen‐activated protein kinase (MAPK) remain active—a bias that may underlie the diverse clinical manifestations of TSHB defects. Structural modeling further demonstrates that both the native and splice variant TSHB proteins effectively interact with the TSH receptor, solidifying their physiological relevance in health and disease."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Harald Brumm, Arne Pfeufer, Heike Biebermann, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Compound heterozygous and homozygous mutations of the TSHbeta gene as a cause of congenital central hypothyroidism in Europe."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Horm Res (2004)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1159/000080071"}], "href": "https://doi.org/10.1159/000080071"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "15297803"}], "href": "https://pubmed.ncbi.nlm.nih.gov/15297803"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Shunsuke Miyai, Shinichi Yoshimura, Yasumasa Iwasaki, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Induction of GH, PRL, and TSH beta mRNA by transfection of Pit-1 in a human pituitary adenoma-derived cell line."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell Tissue Res (2005)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1007/s00441-005-0033-z"}], "href": "https://doi.org/10.1007/s00441-005-0033-z"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "16133148"}], "href": "https://pubmed.ncbi.nlm.nih.gov/16133148"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Kristina Loinder, Mats Söderström "}, {"type": "b", "children": [{"type": "t", "text": "An LXXLL motif in nuclear receptor corepressor mediates ligand-induced repression of the thyroid stimulating hormone-beta gene."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Steroid Biochem Mol Biol (2005)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.jsbmb.2005.06.031"}], "href": "https://doi.org/10.1016/j.jsbmb.2005.06.031"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "16216492"}], "href": "https://pubmed.ncbi.nlm.nih.gov/16216492"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "N Benhadi, W M Wiersinga, J B Reitsma, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Higher maternal TSH levels in pregnancy are associated with increased risk for miscarriage, fetal or neonatal death."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Eur J Endocrinol (2009)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1530/EJE-08-0953"}], "href": "https://doi.org/10.1530/EJE-08-0953"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "19273570"}], "href": "https://pubmed.ncbi.nlm.nih.gov/19273570"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Jeremy S Schaefer, John R Klein "}, {"type": "b", "children": [{"type": "t", "text": "A novel thyroid stimulating hormone beta-subunit isoform in human pituitary, peripheral blood leukocytes, and thyroid."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Gen Comp Endocrinol (2009)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.ygcen.2009.04.006"}], "href": "https://doi.org/10.1016/j.ygcen.2009.04.006"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "19364510"}], "href": "https://pubmed.ncbi.nlm.nih.gov/19364510"}]}, {"type": "r", "ref": 7, "children": [{"type": "t", "text": "Gil Atzmon, Nir Barzilai, Martin I Surks, et al. 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