Supplementary Materials

Supplementary Materials for:

Huntingtin promotes mTORC1 signaling in the pathogenesis of Huntington's disease

William M. Pryor, Marta Biagioli, Neelam Shahani, Supriya Swarnkar, Wen-Chin Huang, Damon T. Page, Marcy E. MacDonald, Srinivasa Subramaniam*

*Corresponding author. E-mail: ssubrama{at}scripps.edu

This PDF file includes:

  • Fig. S1. Effect of normal and expanded poly-Q Htt on amino acid–induced mTORC1 activation.
  • Fig. S2. Expanded poly-Q Htt fragment–mediated mTORC1 is abrogated by an Akt inhibitor.
  • Fig. S3. Expanded poly-Q Htt fragment does not potentiate phosphorylation of mTOR at Ser2448.
  • Fig. S4. Htt depletion inhibits Rheb-mediated mTORC1 activation.
  • Fig. S5. More FL-HTT-86Q than FL-HTT-23Q binds Rheb.
  • Fig. S6. Rheb binds Htt in striatal cells.
  • Fig. S7. Htt colocalizes with LAMP1.
  • Fig. S8. AAV-GFP expression in the striatum of a TSC1flox/+/HD mouse.
  • Fig. S9. Cre injection in TSC1flox/+/wild-type mice elicits mTORC1 activity.
  • Fig. S10. TSC1flox/+/HD mice injected with AAV-Cre show severe weight loss.

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Citation: W. M. Pryor, M. Biagioli, N. Shahani, S. Swarnkar, W.-C. Huang, D. T. Page, M. E. MacDonald, S. Subramaniam, Huntingtin promotes mTORC1 signaling in the pathogenesis of Huntington's disease. Sci. Signal. 7, ra103 (2014).

© 2014 American Association for the Advancement of Science