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J. Biol. Chem., Vol. 280, Issue 21, 20549-20557, May 27, 2005

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RNA CUG-binding Protein 1 Increases Translation of 20-kDa Isoform of CCAAT/Enhancer-binding Protein by Interacting with the and Subunits of Eukaryotic Initiation Translation Factor 2^*

Nikolai A. Timchenko, Gou-Li Wang, and Lubov T. Timchenko

From the Department of Pathology and Huffington Center on Aging, Departments of Medicine and Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, Texas 77030

Expression of a dominant negative 20-kDa isoform of CCAAT/enhancer-binding protein (C/EBP), LIP, is increased in proliferating livers and in tumor cells. Two RNA-binding proteins, CUGBP1 and calreticulin, have been implicated in the translational regulation of C/EBP. In this paper, we present evidence showing several critical steps by which liver increases translation of LIP after partial hepatectomy. At early stages after partial hepatectomy, liver activates CUGBP1 by a hyperphosphorylation. The activated CUGBP1 binds to the 5' region of C/EBP mRNA and replaces calreticulin, which partially represses translation of C/EBP in quiescent livers. The hyperphosphorylated CUGBP1 also interacts with the and subunits of initiation factor eIF2. Our data demonstrate that the interaction of CUGBP1 with the eIF2 enhances the association of CUGBP1 with ribosomes and correlates with increased translation of LIP in the liver after partial hepatectomy. Our data support the hypothesis that CUGBP1 increases translation of LIP by the interaction with the eIF2 subunit. This facilitates subsequent recruitment of larger numbers of ribosomes to initiate translation of LIP.

Received for publication, August 19, 2004 , and in revised form, March 11, 2005.

^* This work was supported by National Institutes of Health Grants GM55188, CA100070, and AG20752 (to N. A. T.) and AR49222 and AR44387 (to L. T. T.) and by grants from the Muscular Dystrophy Association (to L. T. T.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. Tel.: 713-798-6911; Fax: 713-798-3142; E-mail: lubovt{at}bcm.tmc.edu.

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