Expression of GIRK (Kir3.1/Kir3.4) channels in mouse fibroblast cells with and without beta1 integrins.
G protein-activated K+ channel (GIRK) subunits possess a conserved extracellular integrin-binding motif (RGD) and bind directly to beta1 integrins. We expressed GIRK1/GIRK4 channels labeled with green fluorescent protein in fibroblast cell lines expressing or lacking beta1 integrins. Neither plasma membrane localization nor agonist-evoked GIRK currents were affected by the absence of beta1 integrins or by incubation with externally applied RGD-containing peptide. Mutation of the aspartate (D) of RGD impaired currents, GIRK glycosylation, and membrane localization, but the interaction with beta1 integrins remained intact. Thus, beta1 integrins are not essential for functional GIRK expression; and the GIRK-integrin interactions involve structural elements other than the RGD motif.
Ivanina
T
T
Division of Biology, California Institute of Technology, Pasadena 91125, USA.
Neusch
C
C
Li
Y X
YX
Tong
Y
Y
Labarca
C
C
Mosher
D F
DF
Lester
H A
HA
D000818:Animals; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D051676:G Protein-Coupled Inwardly-Rectifying Potassium Channels; D019012:Integrin beta1 / Q000378:metabolism*; D051379:Mice; D009842:Oligopeptides / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism*; D024661:Potassium Channels, Inwardly Rectifying; D011233:Precipitin Tests; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D013347:Subcellular Fractions / Q000378:metabolism
D051676:G Protein-Coupled Inwardly-Rectifying Potassium Channels; D019012:Integrin beta1; D009842:Oligopeptides; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D011993:Recombinant Fusion Proteins; C047981:arginyl-glycyl-aspartic acid