ABSTRACT Structural Feature and Function <strong>of</strong> hβ-subunits <strong>of</strong> BK Channel Jiuping Ding Key Laboratory <strong>of</strong> Molecular Biophysics Ministry <strong>of</strong> Education, College <strong>of</strong> Life Science and Technology, Huazhong University <strong>of</strong> Science and Technology, Wuhan, Hubei, 430074, China The functional diversity <strong>of</strong> large conductance Ca 2+ - and voltage-dependent K + (BK) channels arises mainly from co-assembly <strong>of</strong> the pore-forming mSlo α subunits with four tissue enriched auxiliary β subunits. The structural basis <strong>of</strong> the interaction between α subunits with β subunits is not well understood. Using immun<strong>of</strong>luorescence and patch clamp techniques, we demonstrated that 1) four-turn α-helical segment prevents surface expression <strong>of</strong> the auxiliary hβ2 subunit <strong>of</strong> BK-type channel; 2) lysine-rich extracellular rings formed by hβ2 subunits confer the outward rectification <strong>of</strong> BK channels; 3) structural basis for toxin resistance <strong>of</strong> β4-associated calcium-activated potassium (BK) channels. Those findings provide a better understanding <strong>of</strong> the structure and the diverse interactions between α and β subunits and will improve the design <strong>of</strong> channel inhibitors.
INVITED SPEAKER’S INFO Pr<strong>of</strong>. Jianzhi Wang PhD, Pr<strong>of</strong>essor, Director, Pr<strong>of</strong>essor and Director <strong>of</strong> Pathophysiology Pathophysiology Department, Tongji Medical College, Huazhong University <strong>of</strong> Science and Technology Wuhan, Hubei Province, 430074 P.R.China Email: wangjz@mails.tjmu.edu.cn Education and Training 1975-1978 General Medicine, Tongji (Wuhan) Medical College, Wuhan, China 1985-1988 Post Graduate Training in Biochemistry, Tongji Medical University, Wuhan, China 1992-1993 Postdoctoral Research in Biochemistry, Siena University, Siena, Italy 1993-1996 Postdoctoral Research in Alzheimer disease, NYS Institute for Basic Research, SI, NY, USA Selected Publications 1. Zhu LQ, Zheng HY, Peng CX, Liu D, Li HL, Wang Q and Wang JZ*. Protein Phosphatase 2A Facilitates Axonogenesis by Dephosphorylating CRMP2. J Neurosci. 30(10):3839 –48, 2010 2. Zhu LQ, Liu D, Hu J, Cheng J, Wang SH, Wang Q, Wang F, Chen JG, and Wang JZ*. GSK-3 inhibits presynaptic vesicle exocytosis by phosphorylating P/Q-type calcium channel and interrupting SNARE complex formation. J Neurosci. 30(10):3849 –55, 2010 3. Wang JZ*, Liu F. Microtubule-associated protein tau in development, degeneration and protection <strong>of</strong> neurons. Prog Neurobiol. 85:148-75, 2008 An invited review 4. Li HL, Wang HH, Liu SJ, Deng YQ, Zhang YJ, Tian Q, Wang XC, Chen XQ, Yang Y, Zhang JY, Wang Q, Xu H, Liao F and Wang JZ*. Phosphorylation <strong>of</strong> tau antagonizes apoptosis by stabilizing -catenin, a mechanism involved in Alzheimer’s neurodegeneration. Proc Natl Acad Sci U S A. 104(9): 3591-3596, 2007 5. Zhu LQ, Wang SH, Yin YY, Liu D, Zheng HY, Shi HR, Tian Q, Wang XC, Wang Q, Guo L, Wang JZ*. Activation <strong>of</strong> glycogen synthase kinase-3 inhibits long term potentiation with synapse-associated impairments. J Neurosci. 27,12211–20, 2007 6. Wang D, Qian L, Xiong H, Liu J, Neckameyer WS, Oldham S, Xia K, Wang J, Bodmer R, Zhang Z.Antioxidants protect PINK1-dependent dopaminergic neurons in Drosophila. Proc Natl Acad Sci U S A. 103:13520-5,2006 7. Liu SJ, Zhang JY, Li HJ, Fang ZY, Wang Q, Deng HM, Gong C, Iqbal K, Wang JZ*. Tau becomes a more favorable substrate for GSK-3 when it is