Skip Navigation

This Article
Right arrow Print PDF (11049K)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Concordet, J.-P.
Right arrow Articles by Daegelen, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Concordet, J.-P.
Right arrow Articles by Daegelen, D.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 1991, Vol. 19, No. 15 4173-4180
© 1991


MOLECULAR BIOLOGY

A ubiquitous enhancer shared by two promoters in the human aldolase A gene

Jean-Paul Concordet, Pascal Maire, Axel Kahn and Dominique Daegelen

ICGM, INSERM U129, 24 rue du Fbg St Jacques, 75014 Paris, France

Received April 18, 1991. Revised July 3, 1991. Accepted July 3, 1991.

The human aldolase A gene is transcribed from three different promoters, which are all clustered within a 1.6 kbp DNA domain. Two of these, PN and PH, are ubiquitous and seem to be co-regulated in most tissues while the third one, PM, is specific to adult skeletal muscle. We investigated the sequences involved in the ubiquitous activity of the PN and PH promoters of the human aldolase A gene. Deletion analysis, performed by transient expression assays of chloramphenicol acetyltransferase reporter genes in human HepG2 hepatoma cells, indicated that PH activity results from the interaction of an upstream activating region with two distinct core promoters. The upstream activating region was able to stimulate transcription from the HSV tk promoter as efficiently as the SV40 enhancer in all cell types tested. It appears, therefore, to be a strong ubiquitous enhancer. DNAsel footprinting revealed protections covering sequences scattered along the enhancer, including Sp1 and AP1 motifs. Importantly, we found that this enhancer was also necessary to activity of the other ubiquitous promoter of the aldolase A gene, PN. These studies demonstrate that expression of the human aldolase A gene is mediated by a complex interplay of enhancer and promoter elements.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
H. Jiang, C. S. Okamura, and M. C. Lucy
Isolation and Characterization of a Novel Promoter for the Bovine Growth Hormone Receptor Gene
J. Biol. Chem., March 19, 1999; 274(12): 7893 - 7900.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
A. Lupo, P. Costanzo, L. Medugno, I. Romeo, F. Salvatore, and P. Izzo
Negative Regulation of the Mouse Aldolase A Gene. A CELL CYCLE-DEPENDENT DNA BINDING ACTIVITY FUNCTIONS AS A SILENCER OF GENE TRANSCRIPTION
J. Biol. Chem., December 12, 1997; 272(50): 31641 - 31647.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
G. L. Semenza, B.-H. Jiang, S. W. Leung, R. Passantino, J.-P. Concordet, P. Maire, and A. Giallongo
Hypoxia Response Elements in the Aldolase A, Enolase 1,and Lactate Dehydrogenase A Gene Promoters Contain Essential Binding Sites for Hypoxia-inducible Factor 1
J. Biol. Chem., December 20, 1996; 271(51): 32529 - 32537.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
V. Lacronique, S. Lopez, L. Miquerol, A. Porteu, A. Kahn, and M. Raymondjean
Identification and Functional Characterization of an Erythroid-specific Enhancer in the L-type Pyruvate Kinase Gene
J. Biol. Chem., June 23, 1995; 270(25): 14989 - 14997.
[Abstract] [Full Text] [PDF]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.