Thyrotropin-releasing hormone-stimulated thyrotropin expression involves islet-brain-1/c-Jun N-terminal kinase interacting protein-1

被引:7
作者
Abe, H
Murao, K
Imachi, H
Cao, WM
Yu, X
Yoshida, K
Wong, NCW
Shupnik, MA
Haefliger, JA
Waeber, G
Ishida, T
机构
[1] Kagawa Univ, Fac Med, Dept Internal Med 1, Kagawa 7610793, Japan
[2] Univ Calgary, Fac Med, Dept Med Biochem, Hlth Sci Ctr, Calgary, AB T2N 4N1, Canada
[3] Univ Calgary, Fac Med, Dept Mol Biol, Hlth Sci Ctr, Calgary, AB T2N 4N1, Canada
[4] Univ Virginia, Dept Internal Med, Div Endocrinol & Metab, Charlottesville, VA 22903 USA
[5] CHU Vaudois, Dept Internal Med, Univ Hosp, CH-1011 Lausanne, Switzerland
关键词
D O I
10.1210/en.2004-0635
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Islet-brain-1 (IB1)/c-Jun N-terminal kinase interacting protein 1 (JIP-1) is a scaffold protein that is expressed at high levels in neurons and the endocrine pancreas. IB1/JIP-1 interacts with the c-Jun N-terminal kinase and mediates the specific physiological stimuli (such as cytokines). However, the potential role of the protein in the pituitary has not been evaluated. Herein, we examined expression of the gene encoding IB1/JIP-1 and its translated product in the anterior pituitary gland and a pituitary cell line, GH3. We then examined the potential role of IB1/JIP-1 in controlling TSH-beta gene expression. Exposure of GH3 cells to TRH stimulated the expression of IB1/JIP-1 protein levels, mRNA, and transcription of the promoter. The increase of IB1/JIP-1 content by transient transfection study of a vector encoding IB1/JIP-1 or by the stimulation of TRH stimulates TSH-beta promoter activity. This effect is not found in the presence of a mutated nonfunctional (IB1S59N)IB1/JIP-1 protein. Together, these facts point to a central role of the IB1/JIP-1 protein in the control of TRH-mediated TSH-beta stimulation.
引用
收藏
页码:5623 / 5628
页数:6
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