期刊
ENDOCRINE RESEARCH
卷 34, 期 1-2, 页码 31-42出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/07435800902911810
关键词
L-thyroxine; Integrin v3; Nongenomic Actions; TR1 Transport
资金
- Charitable Leadership and Beltrone Foundations
Introduction. In CV-1 cells, shuttling from cytoplasm to nucleus of the nuclear thyroid hormone receptor-1 (TR1, TR) is shown in this report to be regulated by extracellular thyroid hormone at a hormone receptor on cell surface integrin v3. Methods. The receptor was introduced into cells as a GFP-TR1 chimera and intracellular movement of the receptor was monitored by confocal microscopy of cells treated with L-thyroxine (T4). Results and Discussion. TR-GFP translocation in the presence of T4 requires activation of extracellular-regulated protein kinases 1/2 (ERK1/2). Inhibition of T4-binding to v3 with anti-v3 or Arg-Gly-Asp (RGD) peptide blocks T4-stimulated GFP-TR nuclear translocation, as do the hormone-binding inhibitor tetraiodothyroacetic acid (tetrac) and the ERK1/2 inhibitor, PD98059. TR1 is an ERK1/2 substrate. Conclusions. Via a nongenomic mechanism initiated at plasma membrane integrin v3, T4-activated ERK1/2 and TR1 move transiently in an immunoprecipitable complex to the nuclei of T4-treated cells.
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