NDLI: Identification of an Inverted CCAAT Box Motif in the Fatty-acid Synthase Gene as an Essential Element for Mediation of Transcriptional Regulation by cAMP

Content Provider	Journal of Biological Chemistry (JBC)
Author	Rangan, Vangipuram S. Oskouian, Babak Smith, Stuart
Abstract	The antagonistic effect of cAMP on the insulin-induced expression of fatty acid synthase (FAS) in liver could be mimicked in vitro using H4IIE hepatoma cells, both by measuring the response of the endogenous FAS gene and by assaying expression of transfected reporter genes containing promoter elements of the FAS gene. 5′-Deletion analysis and replacement mutagenesis revealed that an essential element required for cAMP antagonism of the insulin effect is an inverted CCAAT box located between nucleotides −99 and −92. DNase I footprinting and gel shift analysis revealed that this region can bind a protein present in nuclei of liver and spleen, organs that express high and undetectable levels of FAS, respectively. This protein is not a CCAAT/enhancer-binding protein, C/EBP. Thus, the FAS gene appears unusual in that the sequence element required for transcriptional regulation by cAMP is neither a cAMP response element (CRE) nor a binding site for AP-1, AP-2, or C/EBP. These results suggest that essential to the regulation of FAS transcription by cAMP is the interaction of an inverted CCAAT box motif with a constitutively produced trans-acting factor that either itself undergoes modification in response to cAMP or associates with a protein that is produced or modified by cAMP exposure.
Related Links	http://www.jbc.org/content/271/4/2307.abstract
Ending Page	2312
Starting Page	2307
Page Count	6
File Format	HTM / HTML PDF
ISSN	00219258
Journal	Journal of Biological Chemistry (JBC)
Issue Number	4
Volume Number	271
DOI	10.1074/jbc.271.4.2307
e-ISSN	1083351X
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	1996-01-26
Access Restriction	Open
Subject Keyword	Nucleic Acids, Protein Synthesis, and Molecular Genetics
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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