Person
Papazian, Diane M.
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Biography and Research Interest
Diane Papazian received her B.S. in Chemistry from the University of Michigan and her PhD in Biological Chemistry from Harvard University. She did postdoctoral work in Dr. Lily Jan’s lab at USCF before joining the faculty of the Geffen School of Medicine at UCLA. She is now a Professor in the Department of Physiology.
The Papazian lab is interested in the function and development of the zebrafish nervous system and the neural control of locomotor behaviors. Currently, we are developing a zebrafish model for spinocerebellar ataxia type 13 (SCA13), an autosomal dominant genetic disease in humans. SCA13 is characterized by ataxia, oculomotor abnormalities, and the death of cerebellar neurons. The disease is caused by mutations in the KCNC3 gene, which encodes the voltage-gated Kv3.3 potassium channel. SCA13 occurs in distinct neurodevelopmental and neurodegenerative forms depending on the causative mutation. We are using zebrafish to investigate how SCA13 mutations alter neuronal development, excitability, and viability, and locomotor behavior.
The Papazian lab is interested in the function and development of the zebrafish nervous system and the neural control of locomotor behaviors. Currently, we are developing a zebrafish model for spinocerebellar ataxia type 13 (SCA13), an autosomal dominant genetic disease in humans. SCA13 is characterized by ataxia, oculomotor abnormalities, and the death of cerebellar neurons. The disease is caused by mutations in the KCNC3 gene, which encodes the voltage-gated Kv3.3 potassium channel. SCA13 occurs in distinct neurodevelopmental and neurodegenerative forms depending on the causative mutation. We are using zebrafish to investigate how SCA13 mutations alter neuronal development, excitability, and viability, and locomotor behavior.
Non-Zebrafish Publications
Waters, M.F., Minassian, N.A., Stevanin, G., Figueroa, K.P., Bannister, J.P.A., Nolte, D., Mock, A.F., Evidente, V.G., Fee, D., Müller, U., Dürr, A., Brice, A., Papazian, D.M., and Pulst, S.M. (2006) Mutations in the voltage-gated potassium channel KCNC3 cause degenerative and developmental CNS phenotypes. Nat. Genet. 38, 447-451.Figueroa, K.P.*, Minassian, N.A.*, Stevanin G.*, Waters, M., Garibyan, V., Bürk, K., Brice, A., Dürr, A., Papazian, D.M., and Pulst, S.M. (2010) KCNC3: Phenotype, mutations, channel biophysics—a study of 260 familial ataxia patients. Hum. Mutat. 31, 191-196.