Loss of Huntingtin-Mediated BDNF Gene Transcription in Huntington’s Disease Chiara Zuccato, Andrea Ciammola, Dorotea Rigamonti, Blair R. Leavitt, Donato Goffredo, Luciano Conti, Marcy E. MacDonald, Robert M. Friedlander, Vincenzo Silani, Michael R. Hayden, Tõnis Timmusk, Simonetta Sipione, Elena Cattaneo

Supplemental Figure 1. Levels of exogenous huntingtin in engineered cells. Western blot analysis performed on lysates from parental cells (P) and from two subclones stably overexpressing full-length wild-type and mutant huntingtin (clones 9.2 and 10.6, respectively). Equal loading is demonstrated by tubulin immunoreactive band.

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Supplemental Figure 2. RPA on wild-type littermates (L) and YAC18 and YAC72 mice. Determination of exon I, II, III, and IV BDNF levels by RPA performed on total RNA from cortex (ctx), hippocampus (hip), and striatum (str) isolated from 9-month-old mice.

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Supplemental Figure 3. Expression of other neurotrophins in human cortex. Analysis of NGF, NT3, and CNTF mRNA levels by semi-quantitative radioactive RT-PCR, in sample from frozen frontoparietal cortex obtained from an autopsy of age-matched controls (co in figure) and HD patients. Two patients were analyzed for each group. One of the two measurements is shown. NGF, NT3, and CNTF levels were calculated over the amount of SNAP-25 (synaptosomal associated protein 25) used as a control neuronal marker.

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