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J. Biol. Chem., Vol. 277, Issue 42, 39967-39972, October 18, 2002

This Article Full Text Full Text (PDF) All Versions of this Article: 277/42/39967    most recent M200840200v1 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 Li, J. Articles by Wei, L.-N. Search for Related Content PubMed PubMed Citation Articles by Li, J. Articles by Wei, L.-N. Social Bookmarking                      What's this?

Induction of the Mouse -Opioid Receptor Gene by Retinoic Acid in P19 Cells^*

Jinhua Li, Sung Wook Park, Horace H. Loh, and Li-Na Wei

From the Department of Pharmacology, University of Minnesota Medical School, Minneapolis, Minnesota 55455

The mouse -opioid receptor (KOR) gene is expressed in mouse embryonal carcinoma P19 cells and induced by retinoic acid (RA) within 24 h. An RA-responsive cis-acting element is identified within promoter I of the KOR gene. This element contains a GC box, a putative binding site for transcription factor Sp1. Enhanced binding of Sp1 to this GC box correlates with RA induction of KOR gene. Phosphatase inhibitor (sodium pyrophosphate) decreases RA induction of this promoter, whereas hypophosphorylation of Sp1 results in an increase in its DNA binding affinity to this promoter as demonstrated by in vitro gel retardation and in vivo chromatin immunoprecipitation assays. Consistently, the inhibitor of MEK, PD98058, dose-dependently enhances RA induction of this promoter, suggesting that the ERK signaling pathway is negatively involved in the RA induction of mouse KOR gene activities. Collectively, enhanced binding of Sp1 to promoter I of the KOR gene as a result of inhibiting the ERK pathway contributes to RA induction of this gene in P19.

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