HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 282, Issue 31, 22499-22512, August 3, 2007

This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: 282/31/22499    most recent M703778200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Renna, M. Articles by Remondelli, P. Search for Related Content PubMed PubMed Citation Articles by Renna, M. Articles by Remondelli, P. Social Bookmarking                      What's this?

Regulation of ERGIC-53 Gene Transcription in Response to Endoplasmic Reticulum Stress^*

Maurizio Renna, Maria Gabriella Caporaso, Stefano Bonatti, Randal J. Kaufman^¶1, and Paolo Remondelli²

From the Dipartimento di Scienze Farmaceutiche, Università degli Studi di Salerno, Fisciano-Salerno I-84034, Italy, the Dipartimento di Biochimica e Biotecnologie Mediche, Università degli Studi di Napoli "Federico II," Naples I-80131, Italy, and the ^¶Department of Biological Chemistry and Internal Medicine and the Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor, Michigan 48109

Accumulation of unfolded proteins within the endoplasmic reticulum (ER) activates the unfolded protein response, also known as the ER stress response. We previously demonstrated that ER stress induces transcription of the ER Golgi intermediate compartment protein ERGIC-53. To investigate the molecular events that regulate unfolded protein response-mediated induction of the gene, we have analyzed the transcriptional regulation of ERGIC-53. We found that the ERGIC-53 promoter contains a single cis-acting element that mediates induction of the gene by thapsigargin and other ER stress-causing agents. This ER stress response element proved to retain a novel structure and to be highly conserved in mammalian ERGIC-53 genes. The ER stress response element identified contains a 5'-end CCAAT sequence that constitutively binds NFY/CBF and, 9 nucleotides away, a 3'-end region (5'-CCCTGTTGGCCATC-3') that is equally important for ER stress-mediated induction of the gene. This sequence is the binding site for endogenous YY1 at the 5'-CCCTGTTGG-3' part and for undefined factors at the CCATC 3'-end. ATF6-YY1, but not XBP1, interacted with the ERGIC-53 regulatory region and activated ERGIC-53 ER stress response element-dependent transcription. A molecular model for the transcriptional regulation of the ERGIC-53 gene is proposed.

Received for publication, May 8, 2007

^* This work was supported in part by grants from the Consorzio Interuniversitario per le Biotecnologie 2003 (to S. B.) and the Università di Salerno (ex 60% 2005 and 2006) (to P. R.). Portions of this work were supported by National Institutes of Health Grants HL52173 and HL057346 (to R. J. K.). 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.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Fig. S1.

¹ An investigator of the Howard Hughes Medical Institute.

² To whom correspondence should be addressed: Dipartimento di Scienze Farmaceutiche, Università degli Studi di Salerno, Via Ponte Don Melillo, Fisciano-Salerno, Italy I-84034. Tel.: 39-089-962767; Fax: 39-089-969602; E-mail: premondelli{at}unisa.it.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				J. Li, L. A. Chen, C. M. Townsend Jr., and B. M. Evers PKD1, PKD2, and Their Substrate Kidins220 Regulate Neurotensin Secretion in the BON Human Endocrine Cell Line J. Biol. Chem., February 1, 2008; 283(5): 2614 - 2621. [Abstract] [Full Text] [PDF]

				C. C. Glembotski Endoplasmic Reticulum Stress in the Heart Circ. Res., November 9, 2007; 101(10): 975 - 984. [Abstract] [Full Text] [PDF]