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Molecular variants of KCNQ channels expressed in murine portal vein myocytes: a role in delayed rectifier current.
Susumu Ohya, Gerard P Sergeant, Iain A Greenwood, Burton Horowitz
, 92, 1016-23
We have analyzed the expression of KCNQ genes in murine portal vein myocytes and determined that of the 5 known KCNQ channels, only KCNQ1 was expressed. In addition to the full-length KCNQ1 transcript, a novel spliced form (termed KCNQ1b) was detected that had a 63 amino acid truncation at the C-terminus. KCNQ1b was not detected in heart or brain but represented approximately half the KCNQ1 transcripts expressed in PV. Antibodies specific for KCNQ1a stained cell membranes from portal vein myocytes and HEK cells expressing the channel. However, because the antibodies were generated against an epitope in the deleted, C-terminal portion of the protein, these antibodies did not stain HEK cells expressing KCNQ1b. In murine portal vein myocytes, in the presence of 5 mmol/L 4-aminopyridine, an outwardly rectifying K+ current was recorded that was sensitive to linopirdine, a specific blocker of KCNQ channels. Currents produced by the heterologous expression of KCNQ1a or KCNQ1b were inhibited by similar concentrations of linopirdine, and linopirdine prolonged the time-course of the action potential in isolated portal vein myocytes. Our data suggest that these two KCNQ1 splice forms are expressed in murine portal vein and contribute to the delayed rectifier current in these myocytes.