title: Pharmacological characterization of five cloned voltage-gated K+ channels, types Kv1.1, 1.2, 1.3, 1.5, and 3.1, stably expressed in mammalian cell lines.
abstract: We have analyzed the biophysical and pharmacological properties of five cloned K+ (Kv) channels (Kv1.1, Kv1.2, Kv1.3, Kv1.5, and Kv3.1) stably expressed in mammalian cell lines. Kv1.1 is biophysically similar to a K+ channel in C6 glioma cells and astrocytes, Kv1.3 and Kv3.1 have electrophysiological properties identical to those of the types n and l K+ channels in T cells, respectively, and Kv1.5 closely resembles a rapidly activating delayed rectifier in the heart. Each of these native channels may be formed from the homomultimeric association of the corresponding Kv subunits, and pharmacological compounds that selectively modulate them may be useful for the treatment of neurological, immune, and cardiac disorders. The cell lines described in this report could be used to identify such drugs and we have therefore embarked on a pharmacological characterization of the five cloned channels. The compounds tested in this study include 4-aminopyridine, capsaicin, charybdotoxin, cromakalim, dendrotoxin, diltiazem, D-sotalol, flecainide, kaliotoxin, mast cell degranulating peptide, nifedipine, noxiustoxin, resiniferatoxin, and tetraethylammonium.
authors.affiliation: Department of Physiology and Biophysics, University of California, Irvine 92717.
authors.forename: S
authors.initials: S
authors.lastname: Grissmer
authors.forename: A N
authors.initials: AN
authors.lastname: Nguyen
authors.forename: J
authors.initials: J
authors.lastname: Aiyar
authors.forename: D C
authors.initials: DC
authors.lastname: Hanson
authors.forename: R J
authors.initials: RJ
authors.lastname: Mather
authors.forename: G A
authors.initials: GA
authors.lastname: Gutman
authors.forename: M J
authors.initials: MJ
authors.lastname: Karmilowicz
authors.forename: D D
authors.initials: DD
authors.lastname: Auperin
authors.forename: K G
authors.initials: KG
authors.lastname: Chandy
mesh_terms: D016475:3T3 Cells; D000818:Animals; D001483:Base Sequence; D001578:Benzopyrans / Q000494:pharmacology; D002211:Capsaicin / Q000494:pharmacology; D002460:Cell Line; D002478:Cells, Cultured; D018999:Charybdotoxin; D003001:Cloning, Molecular; D019806:Cromakalim; D004110:Diltiazem / Q000494:pharmacology; D004224:Diterpenes / Q000494:pharmacology; D004546:Elapid Venoms / Q000494:pharmacology; D005424:Flecainide / Q000494:pharmacology; D015640:Ion Channel Gating; D051379:Mice; D008969:Molecular Sequence Data; D009543:Nifedipine / Q000494:pharmacology; D009838:Oligodeoxyribonucleotides; D010455:Peptides / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000235:genetics* / Q000502:physiology; D011758:Pyrroles / Q000494:pharmacology; D012604:Scorpion Venoms / Q000494:pharmacology; D013015:Sotalol / Q000494:pharmacology
chemical_list: D001578:Benzopyrans; D004224:Diterpenes; D004546:Elapid Venoms; D009838:Oligodeoxyribonucleotides; D010455:Peptides; D015221:Potassium Channels; D011758:Pyrroles; D012604:Scorpion Venoms; C072276:kaliotoxin; D019806:Cromakalim; D018999:Charybdotoxin; C008331:mast cell degranulating peptide; C020273:dendrotoxin; C052567:noxiustoxin; C024353:resiniferatoxin; D013015:Sotalol; D004110:Diltiazem; D009543:Nifedipine; D005424:Flecainide; D002211:Capsaicin