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Originally published In Press as doi:10.1074/jbc.M101670200 on May 11, 2001

J. Biol. Chem., Vol. 276, Issue 28, 26057-26065, July 13, 2001
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CaM Kinase II-dependent Suppression of Nicotinic Acetylcholine Receptor delta -Subunit Promoter Activity*

Huibin Tang, Zhengxin Sun, and Daniel GoldmanDagger

From the Mental Health Research Institute and Department of Biological Chemistry, University of Michigan, Ann Arbor, Michigan 48109

Nerve-induced muscle activity suppresses nicotinic acetylcholine receptor (nAChR) gene expression by increasing intracellular calcium levels. This suppression is mediated by nAChR promoter sequences harboring at least 1 E-box (CANNTG) that bind myogenic helix-loop-helix transcription factors. How muscle depolarization or increased calcium mediates changes in nAChR promoter activity is not well understood. In chick muscle, protein kinase C (PKC) activation is necessary for activity-dependent nAChR gene suppression. Similar effects of PKC activation have not been found in mammalian skeletal muscle. Therefore, we used rat primary muscle cultures to screen for other calcium-regulated enzymatic activities that may mediate the effects of muscle activity and calcium on nAChR promoter activity. We report here that calcium/calmodulin-dependent protein kinase II (CaM kinase II) can specifically suppress nAChR promoter activity in mammalian muscle. This regulation was mediated by a single E-box sequence residing in the previously characterized nAChR delta -subunit genes 47-base pair activity-dependent enhancer. In vitro protein/DNA interaction studies suggest that CaM kinase II inhibits binding of the myogenic factor, myogenin, to the delta -promoter 47-base pair activity-dependent enhancer. CaM kinase activity is increased in active muscle and inhibition of this enzymatic activity results in increased nAChR delta -promoter activity. Therefore, CaM kinase II may represent a previously unappreciated activity that participates in coupling muscle depolarization to nAChR gene expression.

* This study was supported by NINDS National Institutes of Health Grant R01 NS25153 and NIA National Institutes of Health Grant PO1 AG10821.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger To whom correspondence should be addressed: Mental Health Research Institute, University of Michigan, 205 Zina Pitcher Place, Ann Arbor, MI 48109. Tel.: 734-936-2057; Fax: 734-647-4130; E-mail: neuroman@umich.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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