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Inhibition of an inward rectifier potassium channel (Kir2.3) by G-protein betagamma subunits.

N A Cohen, Q Sha, E N Makhina, A N Lopatin, M E Linder, S H Snyder, C G Nichols

J. Biol. Chem., 1996 Dec 13 , 271, 32301-5

The molecular basis of G-protein inhibition of inward rectifier K+ currents was examined by co-expression of G-proteins and cloned Kir2 channel subunits in Xenopus oocytes. Channels encoded by Kir2.3 (HRK1/HIR/BIRK2/BIR11) were completely suppressed by co-expression with G-protein betagamma subunits, whereas channels encoded by Kir2. 1 (IRK1), which shares 60% amino acid identity with Kir2.3, were unaffected. Co-expression of Galphai1 and Galphaq subunits also partially suppressed Kir2.3 currents, but Galphat, Galphas, and a constitutively active mutant of Galphail (Q204L) were ineffective. Gbetagamma and Kir2.3 subunits were co-immunoprecipitated using an anti-Kir2.3 antibody. Direct binding of G-protein betagamma subunits to fusion proteins containing Kir2.3 N terminus, but not to fusion proteins containing Kir2.1 N terminus, was also demonstrated. The results are consistent with suppression of Kir2.3 currents resulting from a direct protein-protein interaction between the channel and G-protein betagamma subunits. When Kir2.1 and Kir2.3 subunits were coexpressed, the G-protein inhibitory phenotype of Kir2.3 was dominant, suggesting that co-expression of Kir2.3 with other Kir subunits might give rise to novel G-protein-inhibitable inward rectifier currents.

http://www.ncbi.nlm.nih.gov/pubmed/8943291