DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ock, Sangmi | ko |
dc.contributor.author | Ahn, Jihyun | ko |
dc.contributor.author | Lee, Seok Hong | ko |
dc.contributor.author | Kang, Hyun | ko |
dc.contributor.author | Offermanns, Stefan | ko |
dc.contributor.author | Ahn, Hwa Young | ko |
dc.contributor.author | Jo, Young Suk | ko |
dc.contributor.author | Shong, Minho | ko |
dc.contributor.author | Cho, Bo Youn | ko |
dc.contributor.author | Jo, Daewoong | ko |
dc.contributor.author | Abel, E. Dale | ko |
dc.contributor.author | Lee, Tae Jin | ko |
dc.contributor.author | Park, Woo Jin | ko |
dc.contributor.author | Lee, In-Kyu | ko |
dc.contributor.author | Kim, Jaetaek | ko |
dc.date.accessioned | 2023-04-12T06:01:50Z | - |
dc.date.available | 2023-04-12T06:01:50Z | - |
dc.date.created | 2023-04-12 | - |
dc.date.created | 2023-04-12 | - |
dc.date.issued | 2013-12 | - |
dc.identifier.citation | FASEB JOURNAL, v.27, no.12, pp.4899 - 4908 | - |
dc.identifier.issn | 0892-6638 | - |
dc.identifier.uri | http://hdl.handle.net/10203/306150 | - |
dc.description.abstract | Although thyroid-stimulating hormone (TSH) is known to be a major regulator of thyroid hormone biosynthesis and thyroid growth, insulin-like growth factor 1 (IGF-1) is required for mediating thyrocyte growth in concert with TSH in vitro. We generated mice with thyrocyte-selective ablation of IGF-1 receptor (TIGF1RKO) to explore the role of IGF-1 receptor signaling on thyroid function and growth. In 5-wk-old TIGF1RKO mice, serum thyroxine (T-4) concentrations were decreased by 30% in concert with a 43% down-regulation of the monocarboxylate transporter 8 (MCT8), which is involved in T-4 secretion. Despite a 3.5-fold increase in circulating concentrations of TSH, thyroid architecture and size were normal. Furthermore, thyrocyte area was increased by 40% in WT thyroids after 10 d TSH injection, but this effect was absent in TSH-injected TIGF1RKO mice. WT mice treated with methimazole and sodium perchlorate for 2 or 6 wk exhibited pronounced goiter development (2.0 and 5.4-fold, respectively), but in TIGF1RKO mice, goiter development was completely abrogated. These data reveal an essential role for IGF-1 receptor signaling in the regulation of thyroid function and TSH-stimulated goitrogenesis. | - |
dc.language | English | - |
dc.publisher | FEDERATION AMER SOC EXP BIOL | - |
dc.title | IGF-1 receptor deficiency in thyrocytes impairs thyroid hormone secretion and completely inhibits TSH-stimulated goiter | - |
dc.type | Article | - |
dc.identifier.wosid | 000329999000024 | - |
dc.identifier.scopusid | 2-s2.0-84890518350 | - |
dc.type.rims | ART | - |
dc.citation.volume | 27 | - |
dc.citation.issue | 12 | - |
dc.citation.beginningpage | 4899 | - |
dc.citation.endingpage | 4908 | - |
dc.citation.publicationname | FASEB JOURNAL | - |
dc.identifier.doi | 10.1096/fj.13-231381 | - |
dc.contributor.localauthor | Shong, Minho | - |
dc.contributor.nonIdAuthor | Ock, Sangmi | - |
dc.contributor.nonIdAuthor | Ahn, Jihyun | - |
dc.contributor.nonIdAuthor | Lee, Seok Hong | - |
dc.contributor.nonIdAuthor | Kang, Hyun | - |
dc.contributor.nonIdAuthor | Offermanns, Stefan | - |
dc.contributor.nonIdAuthor | Ahn, Hwa Young | - |
dc.contributor.nonIdAuthor | Jo, Young Suk | - |
dc.contributor.nonIdAuthor | Cho, Bo Youn | - |
dc.contributor.nonIdAuthor | Jo, Daewoong | - |
dc.contributor.nonIdAuthor | Abel, E. Dale | - |
dc.contributor.nonIdAuthor | Lee, Tae Jin | - |
dc.contributor.nonIdAuthor | Park, Woo Jin | - |
dc.contributor.nonIdAuthor | Lee, In-Kyu | - |
dc.contributor.nonIdAuthor | Kim, Jaetaek | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | MCT8 | - |
dc.subject.keywordAuthor | T-4 | - |
dc.subject.keywordAuthor | hypertrophy | - |
dc.subject.keywordAuthor | proliferation | - |
dc.subject.keywordPlus | GROWTH-FACTOR-I | - |
dc.subject.keywordPlus | THYROTROPIN | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | ASSOCIATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | ABSENCE | - |
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