Neuroscience 2003 Abstract
| Presentation Number: | 209.2 |
|---|---|
| Abstract Title: | Huntingtin-interacting protein hip-1 may be linked to NMDA receptors by the actin cytoskeleton. |
| Authors: |
Fan, M. M. Y.*1
; Icton, C. D.2
; Luo, T.1
; Sornarajah, L.3
; Metzler, M. M.4
; Hayden, M. R.4
; Raymond, L. A.1,2
1Dept. of Psychiatry, Univ. British Columbia, Vancouver, Canada 2BC, 2255 Wesbrook Mall, V6T 1Z3, 3Canada, 2255 Wesbrook Mall, V6T 1Z3, 4Fac. of Med., 2255 Wesbrook Mall, V6T 1Z3, |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Neurodegenerative Disorders -- Trinucleotide Repeat Diseases: Huntington's Disease |
| Session: |
209. Neurodegenerative Disorders: Disease Mechanisms Poster |
| Presentation Time: | Sunday, November 9, 2003 9:00 AM-10:00 AM |
| Location: | Morial Convention Center - Hall F-I, Board # TT1 |
| Keywords: | NEURODEGENERATION, HUNTINGTON'S DISEASE, POLYGLUTAMINE, TRANSGENIC |
Huntington's disease (HD) is a progressive neurodegenerative disorder caused by expansion of a polyglutamine (polyQ) tract in the huntingtin (htt) protein, resulting in selective neuronal loss in the striatum and cortex. Accumulating evidence suggests an involvement of NMDA receptor (NMDAR) overactivation in this process. Since NMDAR localization and function are dependent in part on interactions with cytoplasmic proteins and the actin cytoskeleton, and because various binding partners of htt are involved in regulation of protein trafficking and likely expression, we are investigating possible interactions between htt-interacting proteins and actin-binding proteins. Specifically, the htt-interacting protein HIP1 and actin-crosslinking proteins such as α-actinins contain putative interacting modular domains. Studies in transfected HEK cells suggest the two proteins bind each other (Fan et al., Prog#92.9, SFN 32nd Annual Meeting 2002). Furthermore, fractionation of cortical and striatal tissues from FVB/N mice reveal an overlapping distribution of the two proteins, and the HIP1/α-actinin/NMDAR interaction can also be demonstrated by co-immunoprecipitation in mouse forebrain tissue homogenate. These experiments are being repeated in transgenic mice expressing polyQ-expanded htt to determine effects of the polyQ-expansion on the HIP1/α-actinin interaction. Results from these studies should aid in our understanding of the mechanisms underlying HD pathology.
Supported by CIHR predoctoral fellowship to M.M.Y.F. and operating grant to L.A.R.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
Copyright © 2003-2026 Society for Neuroscience; all rights reserved. Permission to republish any abstract or part of any abstract in any form must be obtained in writing by SfN office prior to publication.
