Namba N, Inagaki N, Gonoi T, Seino Y, Seino S
Division of Molecular Medicine, Center for Biomedical Science, Chiba University, School of Medicine, Japan.
FEBS Lett. 1996 May 20;386(2-3):211-4. doi: 10.1016/0014-5793(96)00445-0.
We have cloned the human genes encoding the inwardly rectifying K+ (Kir) channel subunits, Kir2.2 (hKir2.2) and its variant, termed hKir2.2v. When expressed in Xenopus oocytes, hKir2.2 produced strong inwardly rectifying K+ currents, whereas the expression of hKir2.2v did not elicit significant currents. Coexpression of hKir2.2v with hKir2.2 showed an hKir2.2v inhibition of hKir2.2 K+ currents, indicating that it acts as a negative regulator of hKir2.2 channel activity. Mutational analysis of hKir2.2v and studies of chimeras between hKir2.2 and hKir2.2v suggest that the intracellular C-terminal region of hKir2.2v participates in the negative regulation of the hKir2.2v channel activity.
