Ilya Bezprozvanny, PhD

Professor
Endowed Title: Carl J. and Hortense M. Thomsen Chair in Alzheimer's Disease Research
Physiology
Graduate Program: Integrative Biology
Neuroscience

Contact Information

UT Southwestern Medical Center
5323 Harry Hines Boulevard
Dallas, Texas 75390

Office Phone: 214-645-6000

ilya.bezprozvanny@utsouthwestern.edu

Biography

Dr. Bezprozvanny's research at UT Southwestern focuses on the functional properties and modulation of intracellular Ca2+ release channels and voltage-gated Ca2+ channels. His laboratory developed a major project on structure-function analysis of the inositol trisphosphate receptor (InsP3R). Although the InsP3R had been cloned ten years previously, no one had successfully expressed a functional channel protein. Dr. Bezprozvanny's laboratory was the first to obtain functional recordings of recombinant InsP3R activity in bilayers. His laboratory is taking an advantage of this approach to analyse InsP3R structure-function. While developing this research, he achieved significant conceptual advances in the field of Ca2+ signaling. Most notably, he proposed a novel InsP3R-PIP2 signaling model of Ca2+ wave initiation and identified key determinants of InsP3R1 modulation by Ca2+ and phosphorylation. He also launched another research program on the mechanisms of targeting and localization of voltage-gated Ca2+ channels in neurons. Dr. Bezprozvanny was the first to discover a potential targeting motif required for synaptic targeting of neuronal voltage-gated Ca2+ channels. These results provide novel insights into synaptic function. The long-term goal of his lab is to characterize the functional differences between multiple InsP3R isoforms and to determine structural determinants responsible for their major functional properties.

Education

Graduate SchoolSt. Petersburg Techical Institute - Russia, Cell Biology (1992)
Graduate SchoolLeningrad Polytechnical Institute, Physics (1988)

Research Interests

Alzheimers disease
Calcium channels and synaptic function
Calcium signaling
Huntingtons disease
Neurodegeneration

Publications

Neuronal calcium mishandling and the pathogenesis of Alzheimer’s disease.

Bezprozvanny I, Mattson MP , Trends Neurosci , September 2008; (31(9)):454-63

Familial Alzheimer disease-linked mutations specifically disrupt Ca2+ leak function of presenilin 1.

Nelson O, Tu H, Lei T, Bentahir M, de Strooper B, Bezprozvanny I , J Clin Invest , May 2007; (117(5)):1230-9

Full length mutant huntingtin is required for altered Ca2+ signaling and apoptosis of striatal neurons in the YAC mouse model of Huntington’s disease.

Zhang H, Li Q, Graham RK, Slow E, Hayden MR, Bezprozvanny I , Neurobiol Dis , July 2008; (31(1)):80-8

Dopaminergic signaling and striatal neurodegeneration in Huntington’s disease.

Tang TS, Chen X, Liu J, Bezprozvanny I , J Neurosci , July 2007; (27(30)):7899-910

Elucidating a normal function of huntingtin by functional and microarray analysis of huntingtin-null mouse embryonic fibroblasts.

Zhang H, Das S, Li QZ, Dragatsis I, Repa J, Zeitlin S, Hajnoczky G, Bezprozvanny I , BMC Neurosci , April 2008; (9):38

Professional Associations/Affiliations

American Association for the Advancement of Science, Member

Biophysical Society, Member

Society for Neuroscience, Member

Society of General Physiologists, Member