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The mechanism of this change in FT3/FT4 ratio remains unknown. Objective: We hypothesize that increased type 2 iodothyronine deiodinase (D2) activity in the thyroid gland may explain the higher FT3/FT4 ratio which is frequently observed in patients with abnormal Tg synthesis. Design: We recently identified a compound heterozygous patient (Patient A) with a Tg G2356R mutation and one previously described (C1245R) that is known to cause a defect in intracellular transport of Tg. In the current study, after determining the abnormality caused by G2356R, we measured D2 activity as well as its mRNA level in the thyroid gland. We also measured the thyroidal D2 activity in 3 patients with Tg transport defect and in normal thyroid tissue. Results: Morphological and biochemical analysis of the thyroid gland from Patient A, complemented by a pulse chase experiment revealed that G2356R produces a defect in intracellular Tg transport. 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Thyroglobulin gene mutations producing defective intracellular transport of thyroglobulin are associated with increased thyroidal type 2 iodothyronine deiodinase activity
http://hdl.handle.net/2237/8630
http://hdl.handle.net/2237/86307ed126af-de95-4be8-b7a4-86336fe90fa6
名前 / ファイル | ライセンス | アクション |
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JCEM-rev-Murata.pdf (3.2 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2007-08-06 | |||||
タイトル | ||||||
タイトル | Thyroglobulin gene mutations producing defective intracellular transport of thyroglobulin are associated with increased thyroidal type 2 iodothyronine deiodinase activity | |||||
言語 | en | |||||
その他のタイトル | ||||||
その他のタイトル | High thyroidal D2 activity with Tg mutation (37 characters) | |||||
言語 | en | |||||
著者 |
Kanou, Yasuhiko
× Kanou, Yasuhiko× Hishinuma, Akira× Tsunekawa, Katsuhiko× Seki, Koji× Mizuno, Yutaka× Fujisawa, Haruki× Imai, Tsuneo× Miura, Yoshitaka× Nagasaka, Tetsuro× Yamada, Chizumi× Ieiri, Tamio× Murakami, Masami× Murata, Yoshiharu |
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アクセス権 | ||||||
アクセス権 | open access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | type 2 iodothyronine deiodinase | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | thyroglobulin | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | mutation | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | thyroid gland | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | goiter | |||||
抄録 | ||||||
内容記述 | Context: Most patients with defective synthesis and/or secretion of thyroglobulin (Tg) present relatively high serum free T3 (FT3) concentrations with disproportionately low free T4 (FT4) resulting in a high FT3/FT4 ratio. The mechanism of this change in FT3/FT4 ratio remains unknown. Objective: We hypothesize that increased type 2 iodothyronine deiodinase (D2) activity in the thyroid gland may explain the higher FT3/FT4 ratio which is frequently observed in patients with abnormal Tg synthesis. Design: We recently identified a compound heterozygous patient (Patient A) with a Tg G2356R mutation and one previously described (C1245R) that is known to cause a defect in intracellular transport of Tg. In the current study, after determining the abnormality caused by G2356R, we measured D2 activity as well as its mRNA level in the thyroid gland. We also measured the thyroidal D2 activity in 3 patients with Tg transport defect and in normal thyroid tissue. Results: Morphological and biochemical analysis of the thyroid gland from Patient A, complemented by a pulse chase experiment revealed that G2356R produces a defect in intracellular Tg transport. D2 activity but not type1 deiodinase in thyroid glands of patients with abnormal Tg transport was significantly higher than in normal thyroid glands, whereas D2 mRNA level in Patient A was comparable with that in normal thyroid glands. Furthermore, there was a positive correlation between D2 activity and FT3/FT4 ratios. Conclusion: Increased thyroidal D2 activity in the thyroid gland is responsible for the higher FT3/FT4 ratios in patients with defective intracellular Tg transport. | |||||
言語 | en | |||||
内容記述タイプ | Abstract | |||||
出版者 | ||||||
言語 | en | |||||
出版者 | The Endocrine Society | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプresource | http://purl.org/coar/resource_type/c_6501 | |||||
タイプ | journal article | |||||
出版タイプ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1210/jc.2006-1242 | |||||
ISSN | ||||||
収録物識別子タイプ | PISSN | |||||
収録物識別子 | 0021-972X | |||||
書誌情報 |
en : Journal of Clinical Endocrinology and Metabolism 巻 92, 号 4, p. 1451-1457, 発行日 2007-04 |
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フォーマット | ||||||
application/pdf | ||||||
著者版フラグ | ||||||
値 | author | |||||
URI | ||||||
識別子 | http://hdl.handle.net/2237/8630 | |||||
識別子タイプ | HDL |