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This version published online on September 2, 2004
Endocrinology, doi:10.1210/en.2004-0635
A more recent version of this article appeared on December 1, 2004
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Submitted on May 18, 2004
Accepted on August 26, 2004

TRH-stimulated TSH expression involves Islet-Brain-1/c-Jun N-terminal Kinase Interacting protein-1

Hiroshi Abe, Koji Murao*, Hitomi Imachi, Wen M. Cao, Xiao Yu, Kazuya Yoshida, Norman C.W. Wong, Margaret A. Shupnik, Jacques-Antoine Haefliger, Gérard Waeber, and Toshihiko Ishida

First Department of Internal Medicine, Faculty of Medicine, Kagawa University, 1750-1, Miki-cho, Kita-gun, Kagawa, 761-0793, Japan; Departments of Medicine and Biochemistry & Molecular Biology, Faculty of Medicine, University of Calgary, Health Sciences Center, 3330 Hospital Drive NW, Calgary, Alberta, Canada, T2N 4N1.; Department of Internal Medicine, Division of Endocrinology and Metabolism, University of Virginia, Charlottesville, Virginia 22903, USA; Department of Internal Medicine B, CHUV-University Hospital, 1011 Lausanne, Switzerland

* To whom correspondence should be addressed. E-mail: mkoji{at}kms.ac.jp.

Islet-Brain-1/cJun-N terminal Kinase Interacting protein 1 (IB1/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 (JNK) 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 stimulate TSH-{beta} promoter activity. This effect is not found in presence of a mutated non-functional (IB1S59N) IB1/JIP-1protein. Together, these point to a central role of the IB1/JIP-1 protein in the control of TRH-mediated TSH-{beta} stimulation.
Key words: TSH • TRH • IB1/JIP-1






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