HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Hu, S. Articles by Ali, D. W. Search for Related Content PubMed PubMed Citation Articles by Hu, S. Articles by Ali, D. W.

Variants of the KCNMB3 regulatory subunit of maxi BK channels affect channel inactivation

¹ Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2E9, Canada
² Centre Hospitalier de l’Université de Montréal, Montreal, Quebec H2L 2W5, Canada
³ Université Libre de Bruxelles, Hôpital Erasme, Brussels B-1070, Belgium

The steady-state and kinetic properties of the KCNMB3 regulatory subunits associated with calcium-activated potassium channels (BK channels) are presented. BK channels containing four sequence variants (V1–V4) in the four different isoforms of the ß-subunit (ß3a, ß3b, ß3c, and ß3d) were expressed in Xenopus oocytes. Reconstituted BK channel inactivation ranged from none to around 90% inactivation. In particular, channels expressing the ß3b-V4 variant displayed a right shift in the potassium current voltage-dependence of activation and inactivated to about 30% of the maximum conductance, compared with wild-type ß3b channels that showed no inactivation. When the membrane potential was depolarized, BK channels inactivated with a very rapid time course (2–6 ms). This same variant was previously demonstrated to show subtly higher incidence in patients with idiopathic epilepsy (IE) compared with controls, especially when combined with variant V2 (combined heterozygotes). Furthermore, the gene maps to a region containing a susceptibility factor for this disorder. Taken together, these data suggest that neurons expressing BK channels composed of the ß3b-V4 variant subunit may experience reduced levels of inhibition and may therefore play permissive roles in high levels of neuronal activity that is characteristic of epilepsy.

potassium channel; ß-subunit; activation; epilepsy

This article has been cited by other articles:

				C. Lv, M. Chen, G. Gan, L. Wang, T. Xu, and J. Ding Four-turn {alpha}-Helical Segment Prevents Surface Expression of the Auxiliary h{beta}2 Subunit of BK-type Channel J. Biol. Chem., February 1, 2008; 283(5): 2709 - 2715. [Abstract] [Full Text] [PDF]

				N. Savalli, A. Kondratiev, S. B. de Quintana, L. Toro, and R. Olcese Modes of Operation of the BKCa Channel {beta}2 Subunit J. Gen. Physiol., July 1, 2007; 130(1): 117 - 131. [Abstract] [Full Text] [PDF]

				A. Diez-Sampedro, W. R. Silverman, J. F. Bautista, and G. B. Richerson Mechanism of Increased Open Probability by a Mutation of the BK Channel J Neurophysiol, September 1, 2006; 96(3): 1507 - 1516. [Abstract] [Full Text] [PDF]

				R. Kanjhan, E. J. Coulson, D. J. Adams, and M. C. Bellingham Tertiapin-Q Blocks Recombinant and Native Large Conductance K+ Channels in a Use-Dependent Manner J. Pharmacol. Exp. Ther., September 1, 2005; 314(3): 1353 - 1361. [Abstract] [Full Text] [PDF]