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First published on June 26, 2007; DOI: 10.1124/mol.107.039206

0026-895X/07/7203-499-501$20.00
Mol Pharmacol 72:499-501, 2007

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PERSPECTIVE

The MiRP2-Kv3.4 Potassium Channel: Muscling In on Alzheimer's Disease

Eun Choi, and Geoffrey W. Abbott

Greenberg Division of Cardiology, Department of Medicine and Department of Pharmacology, Cornell University, Weill Medical College, New York, New York

In this issue of Molecular Pharmacology (p. 665), Pannacione et al. provide evidence of a role for the voltage-gated potassium channel {alpha} subunit Kv3.4 and its ancillary subunit MiRP2 in beta-amyloid (Abeta) peptide-mediated neuronal death. The MiRP2-Kv3.4 channel complex—previously found to be important in skeletal myocyte physiology—is now argued to be a molecular correlate of the transient outward potassium current up-regulated by Abeta peptide, considered a significant step in the etiology of Alzheimer's disease. The authors conclude that MiRP2 and Kv3.4 are up-regulated by Abeta peptide in a nuclear factor {kappa}B-dependent fashion at the transcriptional level, and the sea anemone toxin BDS-I is shown to protect against Abeta peptide-mediated cell death by specific blockade of Kv3.4-generated current. The findings lend weight to the premise that specific channels, such as MiRP2-Kv3.4, could hold promise as future therapeutic targets in Alzheimer's disease and potentially other neurodegenerative disorders.

Received June 21, 2007; accepted June 26, 2007

Address correspondence to: Dr. Geoffrey W. Abbott, Starr 463, Greenberg Division of Cardiology, Weill Medical College of Cornell University, 520 East 70th Street, New York, NY 10021. E-mail: gwa2001{at}med.cornell.edu


Related articles in MolPharm:

Up-Regulation and Increased Activity of KV3.4 Channels and Their Accessory Subunit MinK-Related Peptide 2 Induced by Amyloid Peptide Are Involved in Apoptotic Neuronal Death
A. Pannaccione, F. Boscia, A. Scorziello, A. Adornetto, P. Castaldo, R. Sirabella, M. Taglialatela, G. F. Di Renzo, and L. Annunziato
MolPharm 2007 72: 665-673. [Abstract] [Full Text]  





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