Animal Models

Generated and Characterized:

Kv1.4 -/- (C57BL6)

Guo, W., Xu, H., London, B., and Nerbonne, J.M. Molecular basis of transient outward K+ current diversity in mouse ventricular myocytes. Journal of Physiology, London, 521: 587-599 (1999).

Guo, W., Li, H., London, B., and Nerbonne, J.M. Functional consequences of elimination of Ito,f and Ito,s: early afterdepolarizations, atrioventricular block and ventricular arrhythmias in mice lacking Kv1.4 and expressing a dominant-negative Kv4 α subunit. Circulation Research, 87: 73-79 (2000).

Kv1.1SWAPKv1.5 (C57BL6)

London, B., Guo, W., Pan, X.H., Lee, J.S., Shusterman, V., Logothetis, D.A., Nerbonne, J.M., and Hill, J.A. Targeted replacement of Kv1.5 in the mouse leads to loss of the 4 amino pyridine-sensitive component of IK,slow and resistance to drug-induced QT prolongation. Circulation Research, 88: 940-946 (2001).

Kvβ1 -/- (C57BL6)

Aimond, F., Kwak, S., Rhodes, K.J., and Nerbonne, J.M. Accessory Kvbeta1 subunits differentially modulate the functional expression of voltage-gated K+ channels in mouse ventricular myocytes. Circulation Research 96: 451-458 (2005).

Kv4.2 -/- (FVB and C57BL6)

Guo, W., Jung, W.E.D., Marionneau, C., Aimond, F., Xu, H., Yamada, K.A., Demolombe, S., Schwarz, T.L., and Nerbonne, J.M. Targeted deletion of Kv4.2 eliminates Ito,f and results in electrical and molecular remodeling with no evidence of ventricular hypertrophy or myocardial dysfunction. Circulation Research 97: 1342-1350 (2005).

Hu, H.J., Carrasquillo, Y., Karion, F., Jung, W.E., Nerbonne, J.M., Schwarz, T.L., and Gereau, R.W. The Kv4.2 potassium channel alpha subunit is required for pain plasticity. Neuron 50: 89-100 (2006).

Coming:

Kv4.3 -/- (C57BL6)

Kv2.1 -/- (C57BL6)