Naoko Tanese

Biosketch / Results /

Naoko Tanese

Professor, Department of Microbiology
Office of Science & Research

Contact Info

Address
550 First Avenue
New York, NY 10016

212/263-8945
tanesn01@med.nyu.edu


Education

1988-1993 — University of California at Berkeley, PostDoctoral Training
— Columbia University, Graduate Education

Research Summary

Huntington disease (HD) is a devastating disease that strikes affected individuals in mid-life with symptoms such as motor neuron dysfunction, cognitive and psychiatric disturbances that worsen with age. There is no cure for HD and currently available therapies are of limited use. Better understanding of the functions of the disease-causing huntingtin protein and the pathogenic mechanisms involved in the early stages of HD would permit identification of new targets for therapeutic intervention. Studies suggest that other neurodegenerative disorders caused by poly-glutamine expansion may share similar disease mechanisms. Thus, research on HD will likely contribute to the molecular understanding of many diseases of the brain. The gene that is mutated in HD is huntingtin (Htt), which encodes a large ubiquitously expressed protein. Expansion of a triplet CAG repeat sequence in the Htt gene generates a protein with poly-glutamine repeat expansion, which is the cause of HD, an autosomal, dominantly inherited neurodegenerative disorder. Although the pathogenic mechanisms of HD remain unclear, current evidence suggests significant dysfunction of neurons leading to progressive neuronal loss initially in the striatum. Wild-type Htt has been implicated in many cellular functions including regulation of gene expression, endocytosis and microtubule-directed vesicular trafficking in axons and dendrites. We recently reported a new role for Htt in post-transcriptional gene regulation and maintenance of processing bodies / neuronal RNA granules (PNAS 2008:105,10820; JBC 2010:285,13142). Endogenous Htt was found to co-localize and co-traffic with mRNA in dendrites. An emerging body of evidence suggests regulated transport and local translation of mRNA in neurons play a critical role in establishing their connectivity. Our findings implicate normal Htt in these important dynamic processes in neurons. It is possible that mutant Htt perturbs them in some way, contributing to the HD pathogenesis. Our ongoing research focuses on the identification and characterization of proteins and RNA that associate with normal and mutant Htt.

Research Interests

Transcriptional and post-transcriptional regulation of gene expression in health and disease

Combined FISH and immunofluorescent staining methods to co-localize proteins and mRNA in neurons and brain tissue
Ma, Bin; Tanese, Naoko
2013-08-05; 1064-3745,Methods in molecular biology - id: 463542, year: 2013 Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

Proteomic Analysis of Wild-type and Mutant Huntingtin-associated Proteins in Mouse Brains Identifies Unique Interactions and Involvement in Protein Synthesis
Culver, Brady P; Savas, Jeffrey N; Park, Sung K; Choi, Jeong H; Zheng, Shuqiu; Zeitlin, Scott O; Yates, John R 3rd; Tanese, Naoko
2012-07-02; 0021-9258,Journal of biological chemistry - id: 170420, year: 2012 Journal Article

Quantitative analysis of BDNF/TrkB protein and mRNA in cortical and striatal neurons using alpha-tubulin as a normalization factor
Ma, Bin; Savas, Jeffrey N; Chao, Moses V; Tanese, Naoko
2012-07-24; 1552-4922,Cytometry A - id: 173025, year: 2012 Journal Article

Target genes of the largest human SWI/SNF complex subunit control cell growth
Inoue, Hiroko; Giannakopoulos, Stavros; Parkhurst, Christopher N; Matsumura, Tatsushi; Kono, Evelyn A; Furukawa, Takako; Tanese, Naoko
2012-02-05; 1470-8728,Biochemical journal - id: 138119, year: 2011

Huntingtin mediates dendritic transport of I<super>2</super>-actin mRNA in rat neurons
Ma B; Savas JN; Yu M-S; Culver BP; Chao MV; Tanese N
2012-02-05; 2045-2322,Scientific reports - id: 150540, year: 2011