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Originally published In Press as doi:10.1074/jbc.M110771200 on November 27, 2001

J. Biol. Chem., Vol. 277, Issue 6, 4455-4464, February 8, 2002
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GC Box-binding Transcription Factors Control the Neuronal Specific Transcription of the Cyclin-dependent Kinase 5 Regulator p35*

Sarah RossDagger §, Anri TienhaaraDagger §, Ming-Sum LeeDagger ||**, Li-Huei TsaiDagger ||**, and Grace GillDagger Dagger Dagger

From the Dagger  Department of Pathology and || Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115

Cyclin-dependent kinase 5 (cdk5)/p35 kinase activity is highest in post-mitotic neurons of the central nervous system and is critical for development and function of the brain. The neuronal specific activity of the cdk5/p35 kinase is achieved through the regulated expression of p35 mRNA. We have identified a small 200-bp fragment of the p35 promoter that is sufficient for high levels of neuronal specific expression. Mutational analysis of this TATA-less promoter has identified a 17-bp GC-rich element, present twice, that is both required for promoter activity and sufficient for neuronal specific transcription. A GC box within the 17-bp element is critical for both promoter activity and protein-DNA complex formation. The related transcription factors Sp1, Sp3, and Sp4 constitute most of the GC box DNA binding activity in neurons. We have found that both the relative contribution of the Sp family proteins to GC box binding and the transcriptional activity of these proteins is regulated during neuronal differentiation. Thus, our data show that the GC box-binding Sp proteins contribute to the regulation of p35 expression in neurons, suggesting changes in the Sp transcription factors level and activity may contribute to cell type-specific expression of many genes in the central nervous system.

* 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.

§ Supported by a Taplin research fellowship.

Current address: Center for Laboratory Medicine, Tampere University Hospital, P. O. Box 2000, FIN-33521 Tampere, Finland.

** Supported in part National Institutes of Health Grant RO1 GM53049 (to L.-H. T.).

Dagger Dagger To whom correspondence should be addressed: Dept. of Pathology, Harvard Medical School, 200 Longwood Ave., Boston, MA 02115. Tel.: 617-432-0985; Fax: 617-432-1313; E-mail: grace_gill@hms.harvard.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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