MolPharm

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
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 Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Musso, R.
Right arrow Articles by Eva, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Musso, R.
Right arrow Articles by Eva, C.

0026-895X/97/010027-09$3.00/0
Copyright © by The American Society for Pharmacology and Experimental Therapeutics
All rights of reproduction in any form reserved.
MOLECULAR PHARMACOLOGY 51:27-35 (1997).

Regulation of Mouse Neuropeptide Y Y1 Receptor Gene Transcription: A Potential Role for Nuclear Factor-kappa B/Rel Proteins

Rita Musso, Mariagrazia Grilli, Alessandra Oberto, Silvana Ricci Gamalero, and Carola Eva

Institute of Pharmacology and Experimental Therapeutics, Medical School, University of Torino, 10125 Torino, Italy (R.M., A.O., S.R.G., C.E.), and Division of Pharmacology, Department of Biomedical Sciences and Biotechnology, University of Brescia, 25124 Brescia, Italy (M.G.)

We previously isolated a 1.3-kb genomic fragment in the 5'-flanking region of the murine neuropeptide Y (NPY) Y1 receptor gene, which is able to drive the expression of LacZ reporter gene in neuronal cells. We determined the ability of deletion mutants of this region to modulate transcription of the heterologous luciferase gene in the Y1 receptor-expressing neuroblastoma/glioma NG108-15 cells and the Y1 receptor-deficient 293 cells. Results suggest the presence of a cell type-specific core promoter (-399 to -218 from the initiator ATG) and, upstream, of two positive and two negative regulatory elements. Sequence analysis of the Y1 receptor promoter identified two decameric sequences corresponding to consensus binding sites for nuclear factor-kappa B/Rel proteins. Gel shift analysis indicated that a 29-bp oligonucleotide comprising the two putative kappa B sites, which we refer to as Y1-kappa B sequence, specifically binds kappa B-related complexes in nuclear extracts from rat brain areas, NG108-15 cells, and the murine T cell clone A.E7. In nuclear extracts from A.E7 and NG108-15 cells, the Y1-kappa B sequence specifically binds an additional complex whose molecular nature remains to be elucidated. Through transient transfection studies, we also demonstrated that the Y1-kappa B sequence acts as an enhancer element, inferring its potential role in regulation of the Y1 receptor gene expression.

Copyright © by The American Society for Pharmacology and Experimental Therapeutics




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1997 by the American Society for Pharmacology and Experimental Therapeutics