ZFIN ID: ZDB-PERS-100614-2
Papazian, Diane M.
Email: Papazian@mednet.ucla.edu
URL: http://www.physiology.ucla.edu/Labs/Papazian/WebPage/Homepage/Diane_Papazian_Homepage.html
Affiliation: Papazian Lab
Address: Professor Department of Physiology David Geffen School of Medicine University of California at Los Angeles Box 951751 Los Angeles, CA 90095-1751 USA
Country: United States
Phone: (310) 206-7043
Fax: (310) 206-5661
ORCID ID:


BIOGRAPHY AND RESEARCH INTERESTS
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.


PUBLICATIONS
Hsieh, J.Y., Papazian, D.M. (2018) In Vivo Analysis of Potassium Channelopathies: Loose Patch Recording of Purkinje Cell Firing in Living, Awake Zebrafish. Methods in molecular biology (Clifton, N.J.). 1684:237-252
Hsieh, J., Ulrich, B., Issa, F.A., Wan, J., Papazian, D.M. (2014) Rapid development of Purkinje cell excitability, functional cerebellar circuit, and afferent sensory input to cerebellum in zebrafish. Frontiers in neural circuits. 8:147
Issa, F.A., Mock, A.F., Sagasti, A., and Papazian, D.M. (2012) Spinocerebellar ataxia type 13 mutation associated with disease onset in infancy disrupts axonal pathfinding during neuronal development. Disease models & mechanisms. 5(6):921-929
Issa, F.A., Mazzochi, C., Mock, A.F., and Papazian, D.M. (2011) Spinocerebellar ataxia type 13 mutant potassium channel alters neuronal excitability and causes locomotor deficits in zebrafish. The Journal of neuroscience : the official journal of the Society for Neuroscience. 31(18):6831-6841
Issa, F.A., O'Brien, G., Kettunen, P., Sagasti, A., Glanzman, D.L., Papazian, D.M. (2011) Neural circuit activity in freely behaving zebrafish (Danio rerio). The Journal of experimental biology. 213(Pt 6):1028-1038
Mock, A.F., Richardson, J.L., Hsieh, J.Y., Rinetti, G., and Papazian, D.M. (2010) Functional effects of spinocerebellar ataxia type 13 mutations are conserved in zebrafish Kv3.3 channels. BMC Neuroscience. 11(1):99

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.