期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 411, 期 C, 页码 86-96出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2015.04.014
关键词
Thyroid hormone receptor; Thyroid hormone; Nuclear export; Exportin
资金
- National Institutes of Health [2R15DK058028-03]
- National Science Foundation [MCB 1120513]
- Div Of Molecular and Cellular Bioscience
- Direct For Biological Sciences [1120513] Funding Source: National Science Foundation
The thyroid hormone receptor (TR) undergoes nucleocytoplasmic shuttling and regulates target genes involved in metabolism and development. Previously, we showed that TR follows a CRM1/calreticulin-mediated nuclear export pathway. However, two lines of evidence suggest TR also follows another pathway: export is only partially blocked by leptomycin B (LMB), a CRM1-specific inhibitor; and we identified nuclear export signals in TR that are LMB-resistant. To determine whether other exportins are involved in TR shuttling, we used RNA interference and fluorescence recovery after photobleaching shuttling assays in transfected cells. Knockdown of exportins 4, 5, and 7 altered TR shuttling dynamics, and when exportins 5 and 7 were overexpressed, TR distribution shifted toward the cytosol. To further assess the effects of exportin overexpression, we examined transactivation of a TR-responsive reporter gene. Our data indicate that multiple exportins influence TR localization, highlighting a fine balance of nuclear import, retention, and export that modulates TR function. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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