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Papers In Press, published online ahead of print April 20, 2004
Department of Biochemistry and Molecular Biology, University of Florida, Gainesville, FL 32610-0245
Corresponding Author: mkilberg{at}ufl.edu
CCAAT/enhancer-binding protein b (C/EBP
J. Biol. Chem, 10.1074/jbc.M313920200
Submitted on December 19, 2003
Revised on April 20, 2004
Accepted on April 20, 2004
Human CCAAT/enhancer-binding protein beta (C/EBP
) gene expression is activated by endoplasmic reticulum stress through an unfolded protein response element downstream of the protein coding sequence
) is a member of the bZIP family of transcription factors that contribute to the regulation of a wide range of important cellular processes. The data in the present study documents that transcription from the human C/EBP gene is induced in response to endoplasmic reticulum stress, such as glucose deprivation, or treatment of cells with tunicamycin or thapsigargin. Transient transfection of C/EBP genomic fragments linked to a luciferase reporter gene demonstrated that the C/EBP promoter plays no major regulatory role. Instead, by deletion analysis it was discovered that a 46 bp region, located at a genomic site that corresponds to the 3’ untranslated region of the C/EBP mRNA, harbored an element that was required for the stress response. Mutagenesis demonstrated that a cis-regulatory element located at nt +1614 to 1621 (5'-TGACGCAA-3') is responsible for activation of the C/EBP gene. This element is homologous to a previously reported mammalian unfolded protein response element (mUPRE) that binds XBP1. Consistent with those data, over-expression of XBP1 caused an increase in transcription that was mediated by the C/EBP mUPRE.
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