Rhes, a striatal-enriched small G protein, mediates mTOR signaling and L-DOPA-induced dyskinesia

Srinivasa Subramaniam; Francesco Napolitano; Robert G. Mealer; Seyun Kim; Francesco Errico; Roxanne Barrow; Neelam Shahani; Richa Tyagi; Solomon H. Snyder; Alessandro Usiello

doi:10.1038/nn.2994

Rhes, a striatal-enriched small G protein, mediates mTOR signaling and L-DOPA-induced dyskinesia

Srinivasa Subramaniam, Francesco Napolitano, Robert G. Mealer, Seyun Kim, Francesco Errico, Roxanne Barrow, Neelam Shahani, Richa Tyagi, Solomon H. Snyder, Alessandro Usiello

School of Medicine

Research output: Contribution to journal › Article

Abstract

L-DOPA-induced dyskinesia, the rate-limiting side effect in the therapy of Parkinson's disease, is mediated by activation of mammalian target of rapamycin (mTOR) signaling in the striatum. We found that Rhas ^-/- homolog enriched in striatum (Rhes), a striatal-specific protein, binds to and activates mTOR. Moreover, Rhes mice showed reduced striatal mTOR signaling and diminished dyskinesia, but maintained motor improvement on L-DOPA treatment, suggesting a therapeutic benefit for Rhes-binding drugs.

Original language	English (US)
Pages (from-to)	191-193
Number of pages	3
Journal	Nature neuroscience
Volume	15
Issue number	2
DOIs	https://doi.org/10.1038/nn.2994
State	Published - Feb 1 2012

ASJC Scopus subject areas

Neuroscience(all)

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Subramaniam, S., Napolitano, F., Mealer, R. G., Kim, S., Errico, F., Barrow, R., Shahani, N., Tyagi, R., Snyder, S. H., & Usiello, A. (2012). Rhes, a striatal-enriched small G protein, mediates mTOR signaling and L-DOPA-induced dyskinesia. Nature neuroscience, 15(2), 191-193. https://doi.org/10.1038/nn.2994

Rhes, a striatal-enriched small G protein, mediates mTOR signaling and L-DOPA-induced dyskinesia. / Subramaniam, Srinivasa; Napolitano, Francesco; Mealer, Robert G.; Kim, Seyun; Errico, Francesco; Barrow, Roxanne; Shahani, Neelam; Tyagi, Richa ; Snyder, Solomon H.; Usiello, Alessandro.

In: Nature neuroscience, Vol. 15, No. 2, 01.02.2012, p. 191-193.

Research output: Contribution to journal › Article

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