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This version published online on February 24, 2005
Endocrinology, doi:10.1210/en.2004-1662
A more recent version of this article appeared on June 1, 2005
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Submitted on December 27, 2004
Accepted on February 15, 2005

Blockade of rapid versus prolonged ERK1/2 activation has differential effects on insulin-induced gene expression

Adam B. Keeton, Katherine D. Bortoff, J. Lee Franklin, and Joseph L. Messina*

Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, Birmingham AL, 35294-0019

* To whom correspondence should be addressed. E-mail: messina{at}path.uab.edu.

In the present work, insulin's regulation of expression of the transcription factor ATF-3, the putative transcription factor Pip92, and of Insig-1 (an ER resident protein involved in regulation of SREBP-1 activation) have been examined in a liver derived cell line (rat H4IIE hepatoma cells). We report that: (1) Insulin-induced transcription of ATF-3, Pip92, and Insig-1 required MEK-ERK activation (2). Insulin-induced transcription of ATF-3 and Pip92 reached maximum levels within 15 min., and was blocked by wortmannin but not LY294002 (3). In contrast, the maximum level of insulin-induced transcription of Insig-1 was delayed and was not blocked by either wortmannin or LY294002 (4). Insulin activated ERK1/2 in two distinct phases, a rapid peak and a later plateau (5). The delayed plateau phase of insulin-induced ERK1/2 activation was partially PI3-K dependent (6). However the rapid, insulin-induced peak of ERK1/2 activation was blocked by wortmannin, but not LY294002.
Key words: Insulin • ERK • ATF-3 • Pip92 • Insig-1 • PI3-Kinase




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