| Item type |
文献 / Documents(1) |
| 公開日 |
2016-02-29 |
| アクセス権 |
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アクセス権 |
open access |
| 資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
| 出版社版DOI |
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識別子タイプ |
URI |
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関連識別子 |
http://www.jci.org/articles/view/10523/version/1/pdf/render |
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言語 |
ja |
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|
関連名称 |
10.1172/JCI10523 |
| 出版タイプ |
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|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
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タイトル |
Primary hyperparathyroidism caused by parathyroid-targeted overexpression of cyclin D1 in transgenic mice |
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言語 |
en |
| 著者 |
イマニシ, ヤスオ
細川, 義隆
吉本, 勝彦
Schipani, Ernestina
Mallya, Sanjay
Papanikolaou, Alexandros
Kifor, Olga
トクラ, タケヒコ
Sablosky, Marilyn
Ledgard, Felicia
Gronowicz, Gloria
Wang, Timothy C.
Schmidt, Emmett V.
Hall, Charles
Brown, Edward M.
Bronson, Roderick
Arnold, Andrew
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| 抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
The relationship between abnormal cell proliferation and aberrant control of hormonal secretion is a fundamental and poorly understood issue in endocrine cell neoplasia. Transgenic mice with parathyroid-targeted overexpression of the cyclin D1 oncogene, modeling a gene rearrangement found in human tumors, were created to determine whether a primary defect in this cell-cycle regulator can cause an abnormal relationship between serum calcium and parathyroid hormone response, as is typical of human primary hyperparathyroidism. We also sought to develop an animal model of hyperparathyroidism and to examine directly cyclin D1’s role in parathyroid tumorigenesis. Parathyroid hormone gene regulatory region–cyclin D1 (PTH–cyclin D1) mice not only developed abnormal parathyroid cell proliferation, but also developed chronic biochemical hyperparathyroidism with characteristic abnormalities in bone and, notably, a shift in the relationship between serum calcium and PTH. Thus, this animal model of human primary hyperparathyroidism provides direct experimental evidence that overexpression of the cyclin D1 oncogene can drive excessive parathyroid cell proliferation and that this proliferative defect need not occur solely as a downstream consequence of a defect in parathyroid hormone secretory control by serum calcium, as had been hypothesized. Instead, primary deregulation of cell-growth pathways can cause both the hypercellularity and abnormal control of hormonal secretion that are almost inevitably linked together in this common disorder. |
|
言語 |
en |
| 書誌情報 |
en : Journal of Clinical Investigation
巻 107,
号 9,
p. 1093-1102,
発行日 2001-05
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| 収録物ID |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
00219738 |
| 収録物ID |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AA00695520 |
| 権利情報 |
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|
言語 |
en |
|
権利情報 |
Copyright © 2001, American Society for Clinical Investigation |
| EID |
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識別子 |
72261 |
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識別子タイプ |
URI |
| 言語 |
|
|
言語 |
eng |
LID201602262008.pdf (2.72 MB)
