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Roberto Zayas

Ph.D. 2005

Thesis Title: Calcium Entry and Calcium-Mediated Mechanisms in the Slow-Channel Syndrome

E-mail: zaya0001@umn.edu

Advisor: Christopher M. Gomez

Thesis Publications:

“Inositol-1,4,5-triphosphate receptors mediate activity-induced subsynaptic
Ca2+ signals in muscle fibers and Ca2+ overload in slow-channel syndrome”.
Zayas R, Groshong J, Gomez C. In press Journal of Cell Calcium.

“Macroscopic properties of spontaneous mutations in SCS: correlation by domain and disease severity”. Zayas R, Gomez C. Synapse. 2006 Jul 31;60(6):441-449.

“Apoptotic pathways at muscle fiber synapses are circumscribed, non-lethal, and reversible”. Vohra B, Groshong J, Zayas R, Gomez C. Neurobiology of Disease. 2006 Aug;23(2):462-70.

“Acetylcholine receptor mutations in slow-channel syndrome identify an M1 domain allosteric hinge”. Navedo MF, Lasalde-Dominicci JA, Báez-Pagán C, Díaz-Pérez L, Rojas L, Maselli RA., Staub J, Schott K, Zayas R, Gomez CM.
Journal of Molecular and Cellular Neuroscience. 2006 May-Jun;32(1-2):82-90.

“Novel beta subunit mutation causes a slow-channel syndrome by enhancing activation and decreasing the rate of agonist dissociation.” Navedo MF, Lasalde-Dominicci JA, Baez-Pagan CA, Diaz-Perez L, Rojas LV, Maselli RA, Staub J, Schott K, Zayas R, Gomez CM. Molecular Cellular Neuroscience. 2006 May-Jun;32(1-2):82-90.

“Active calcium accumulation underlies severe weakness in a panel of mice with slow-channel syndrome”. Gomez C, Maselli R, Groshong J, Zayas R, Wollmann RL, Cens T, Charnet P. Journal of Neuroscience. 2002 Aug 1; 22(15):
6447-57.

“Calpain activation impairs neuromuscular transmission in a mouse model of the slow-channel myasthenic syndrome”. Groshong J, Zayas R, Gomez C.
Submitted.

Present Position:

Juris Doctor Student
William Mitchell College of Law