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J. Biol. Chem., Vol. 278, Issue 36, 34691-34699, September 5, 2003

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Mapmodulin/Leucine-rich Acidic Nuclear Protein Binds the Light Chain of Microtubule-associated Protein 1B and Modulates Neuritogenesis^*

Puneet Opal  , Jesus J. Garcia ¶ ||, Friedrich Propst **, Antoni Matilla , Harry T. Orr  and Huda Y. Zoghbi  ¶ ||

From the Departments of Neurology and ^¶Molecular and Human Genetics, ^||Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030, the ^**Institute of Biochemistry and Molecular Cell Biology, Vienna Biocenter, University of Vienna, A-1030 Vienna, Austria, the Medical Molecular Biology Unit, Institute of Child Health, University College, London WC1N 1EH, United Kingdom and the Departments of Laboratory Medicine and Pathology and Biochemistry, and the Institute of Human Genetics, University of Minnesota, Minneapolis, Minnesota 55455

We had previously described the leucine-rich acidic nuclear protein (LANP) as a candidate mediator of toxicity in the polyglutamine disease, spinocerebellar ataxia type 1 (SCA1). This was based on the observation that LANP binds ataxin-1, the protein involved in this disease, in a glutamine repeat-dependent manner. Furthermore, LANP is expressed abundantly in purkinje cells, the primary site of ataxin-1 pathology. Here we focused our efforts on understanding the neuronal properties of LANP. In undifferentiated neuronal cells LANP is predominantly a nuclear protein, requiring a bona fide nuclear localization signal to be imported into the nucleus. LANP translocates from the nucleus to the cytoplasm during the process of neuritogenesis, interacts with the light chain of the microtubule-associated protein 1B (MAP1B), and modulates the effects of MAP1B on neurite extension. LANP thus could play a key role in neuronal development and/or neurodegeneration by its interactions with microtubule associated proteins.

Received for publication, March 19, 2003 , and in revised form, May 23, 2003.

^* This work was supported in part by National Institutes of Health Grants K08 NS02246-03 (to P. O.) and R01 NS27699-13 (to H. Y. Z.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Davee Dept. of Neurology, Northwestern University, Feinberg School of Medicine, Ward Ward 10-332, 303 E. Chicago Ave., Chicago, IL 60611. Tel.: 312-503-4699; Fax: 312-503-0872; E-mail: p-opal{at}northwestern.edu.

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