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Kv4.3, Control Antigen (Kcnd3, Voltage-gated Potassium Channel)

Cat no: K9019A

Kv4.3, Control Antigen (Kcnd3, Voltage-gated Potassium Channel)

Control Antigen for K9019\n\nEpitope: Synthetic linear peptide corresponding to aa451-467 [(C)NEAL ELTGT PEEEH MGK] of human Kv4.3 (Accession NP_004971).\n\nSpecies Sequence Homology: \nRat, rabbit: 100%; Mouse: 16/17.\n\nChloride channels have several functions including: (1) regulating cell volume; (2) membrane potential stabilization; (3) signal transduction; and (4) transepithelial transport. The CLC chloride channel family (which includes voltage-gated chloride channels) represents one of the structural families of chloride channels. Mammals have at least nine different members.5 CLC-2 channels exhibit differential brain distribution and are implicated in regulating and maintaining the chloride gradient in cells that exhibit primarily inhibitory GABAA responses.6 CLC-3 channels are important in cardiac function and their volume sensitivity may be due to PKC/PKA modulated phosphorylation.7 Voltage-gated sodium channels (VGSC) are present in most excitable cells. In neuronal tissue, they are responsible for generating and propagating action potentials. Brain VGSC are heteromers of a1b2 Subunits. Of these, the alpha subunit forms the channel pore. Twelve alpha subunit genes have been identified.8 VGSC have been implicated in numerous neurological and cardiac disorders. Further, VGSC are important in mediating many therapeutic drug effects (including the actions of anesthetics, antiarrhythmics and antiepileptics). 9,10 \n\nPotassium channels contribute to maintaining cell volume, membrane potential, neuronal excitability and the secretion of transmitters, salt and hormones. Two families of potassium channels have been identified. One family includes the inwardly rectifying potassium channels whereas, the other family includes: voltagesensing (KV); big conductance, calcium activated (BKCA); and small conductance, calcium activated (SK) potassium channels. In neuronal tissue, BK and SK channels modulate the action potential duration, the speed of repolarization and the after hyperpolarization. 11,12 These channels are implicated both in therapeutic drug effects and also in disease.11-13 KV channels have been implicated in activity-dependent, plastic changes in neuronal tissue.14,15 HERG (human ether-a-go-go-related gene) is similar to the delayed rectifier channel and is important in cardiac function and may also play a role in certain cardiac arrhythmias.16 Many subunits that form the ion channels have been cloned and expressed. With the combination of molecular biology and electrophysiology, although much has been learned about the structure and function of the ion channels, much remains to be determined about the in vivo physiological roles of the ion channel subtypes and also in their roles in mediating therapeutic drug effects. Monovalent ion channels are being associated with a growing number of diseases.10,17 Thus, further research is required to determine the physiological function and role of Cl, K and Na channel subtypes as well as the ion channels themselves in the hopes of discovering new treatments for these pathologies. \n\nApplications:\nSuitable for use in Antibody Blocking. Not suitable for use in Western Blot due to low molecular weight. Other applications not tested.\n\nRecommended Dilution:\nPreadsorption Control: 1ug peptide per 1ug antibody.\nOptimal dilutions to be determined by researcher.\n\nStorage and Stability: \nLyophilized powder may be stored at 4 degrees C for short-term only. Stable for 12 months at -20 degrees C. Reconstitute to nominal volume (see reconstitution instructions for peptides) and store at -20 degrees C. For maximum recovery of product, centrifuge the original vial prior to removing the cap. Further dilutions can be made in assay buffer.\n\n\n

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SPECIFICATIONS

Catalog Number

K9019A

Size

1mg

Applications

WB

Form

Supplied as a lyophilized powder.\nReconstitution: Reconstitute with 1ml sterile, distilled, deionized water.

Purity

~90%

References

1. Serodio, P., and Rudy, B., J. Neurophysiol., 75, 2174 (1996). 2. Ohya, S., et al., FEBS Lett., 420, 47 (1997). 3. Dixon, J.E., et al., Circ. Res., 79, 659 (1996). 4. Tsaur, M.L., FEBS Lett., 400, 215 (1997). 5. Jentsch, T.J. et al., J. Physiol., 482, 19S, (1995). 6. Staley, K. et al., Neuron, 17, 543, (1996). 7. Nagasaki M. et al., J.Physiol., 523, 705 (2000). 8. Jeong, S.Y. et al., Biochem. Biophys. Res. Commun., 267, 262 (2000). 9. Catterall, W.A., Adv. Neurol., 79, 441 (1999). 10. Vincent, G.M. et al., Cardiol. Rev., 7, 44 (1999). 11. Scholtz, A. et al., J. Physiol., 513, 55 (1998). 12. Dreixler, J.C. et al., Anesth. Analg., 90, 727 (2000). 13. Bond, C.T. et al., Ann. N.Y. Acad. Sci., 868, 370 (1999). 14. Grosse, G. et al., J. Neurosci., 20, 1869 (2000). 15. McFarlane, S. and Pollock, N.S., J. Neurosci., 20, 1020 (2000). 16. Teschemacher, A.G. et al., Br. J. Pharmacol., 128, 479 (1999). 17. Lehmann-Horn, F. and Jurkat-Rott, K., Physiol. Rev., 79, 1317 (1999)

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