These authors contributed equally to this work.
Binding of the repressor complex REST-mSIN3b by small molecules restores neuronal gene transcription in Huntington's disease models
Article first published online: 19 JUL 2013
© 2013 International Society for Neurochemistry
Journal of Neurochemistry
Volume 127, Issue 1, pages 22–35, October 2013
How to Cite
J. Neurochem.(2013) 127, 22–35
- Issue published online: 24 SEP 2013
- Article first published online: 19 JUL 2013
- Accepted manuscript online: 26 JUN 2013 02:20AM EST
- Manuscript Accepted: 17 JUN 2013
- Manuscript Revised: 10 JUN 2013
- Manuscript Received: 26 APR 2013
- STEM-HD. Grant Number: LSHB-CT-2006-037349
- Huntington's Disease Society of America Coalition for the Cure
Figure S1. Luciferase activity in HD NS-HdhQ111/7 cells after transfection with the SRE construct and treatment at different doses of C91 (1nM, 250nM, and 1500nM).
Figure S2. C91 influences Bdnf gene transcription in NS-HdhQ7/7.
Figure S3. C91 does not influence the transcription of non-REST-regulated genes.
Figure S4. Specific localization of mSIN3b in the nucleus of HD heterozygous knock-in NS cells.
Figure S5. Bdnf gene transcription analysis during Zebrafish development.
Figure S6. C91 is not toxic to Zebrafish embryos.
Figure S7. C91 restores the transcription of REST-regulated genes in the HTT knockdown Zebrafish embryo.
Table S1. Luciferase activity and cell viability data obtained from primary screening in DiaNRSELuc8 cells treated with compounds selected by the virtual screening approach.
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