Background: Pore-forming (alpha) subunit of voltage-gated rapidly inactivating A-type potassium channels. May contribute to Icurrent in heart and current in neurons. Channel properties are modulated by interactions with other alpha subunits and with regulatory subunits In response to membrane depolarization, Kv4.2 channels accumulate in the closed-inactivated state(s), from which they directly recover, bypassing the open state. Kv4.2 is a substrate for ERK in vitro and in vivo, and suggest that ERK may regulate potassium-channel function by direct phosphorylation of the pore-forming alpha subunit.
Positive Control: Highly expressed in heart and throughout the brain, with similar levels in cortex and hypothalamus, and much higher levels in hippocampus, dentate gyrus and the habenular nucleus of the thalamus. Detected at similar levels in heart atrium and ventricle. Detected in aorta, cardiac and smooth muscle.
Purification Method: Ammonium Sulfate Precipitation.
Source: Rabbits were immunized with a peptide representing amino acids 453-470 of rat Kv4.2 conjugated to KLH.
Formulation: Provided as solution in phosphate buffered saline with 0.08% sodium azide.
References: 1. Roberds,S.L. et.al, Cloning and tissue-specific expression of five voltage-gated potassium channel cDNAs expressed in rat heart. Proc. Natl. Acad. Sci. U.S.A. 88 (5), 1798-1802 (1991)
2. Bahring, K.et.al. Kinetic analysis of open- and closed-state inactivation transitions in human Kv4.2 A-type potassium channels. J Physiol ;535(Pt 1):65-81 (2001)
3. Adams, T. et.al,The A-type potassium channel Kv4.2 is a substrate for the mitogen-activated protein kinase ERK. J Neurochem 5(6):2277-87 (2000).
UniProt: Q63881.
Caution: This product is intended FOR RESEARCH USE ONLY, and FOR TESTS IN VITRO, not for use in diagnostic or therapeutic procedures involving humans or animals.
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