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.


Graduate School Leningrad Polytechnical Institute (1988), Physics
Graduate School St. Petersburg Techical Institute - Russia (1992), Cell Biology

Research Interest

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


Featured Publications LegendFeatured Publications

Neuronal calcium mishandling and the pathogenesis of Alzheimer’s disease.
Bezprozvanny I, Mattson MP Trends Neurosci September 2008 31(9) 454-63
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
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
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
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

Professional Associations/Affiliations

  • American Association for the Advancement of Science, Member
  • Biophysical Society, Member
  • Society for Neuroscience, Member
  • Society of General Physiologists, Member