Modulation of a recombinant glycine transporter (GLYT1b) by activation of protein kinase C.
Treatment of human embryonic kidney cells (HEK 293 cells) expressing the mouse glycine transporter 1 (GLYT1b) with the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) decreased specific [3H]glycine uptake. This down-regulation resulted from a reduction of the maximal transport rate and was blocked by the PKC inhibitors 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H7) and staurosporine. The inhibitory effect of PMA treatment was also observed after removing all five predicted phosphorylation sites for PKC in GLYT1b by site-directed mutagenesis. These data indicate that glycine transport by GLYT1b is modulated by PKC activation; however, this regulation may involve indirect phosphorylation mechanisms.
Sato
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K
Abteilung Neurochemie, Max-Planck-Institut für Hirnforschung, Frankfurt, Germany.
Adams
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R
Betz
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Schloss
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D026921:Amino Acid Transport Systems, Neutral; D002352:Carrier Proteins / Q000378:metabolism*; D002460:Cell Line; D004789:Enzyme Activation; D005998:Glycine / Q000378:metabolism; D050487:Glycine Plasma Membrane Transport Proteins; D006801:Humans; D008564:Membrane Potentials; D009154:Mutation; D011493:Protein Kinase C / Q000378:metabolism*; D011994:Recombinant Proteins; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D026921:Amino Acid Transport Systems, Neutral; D002352:Carrier Proteins; D050487:Glycine Plasma Membrane Transport Proteins; D011994:Recombinant Proteins; C493268:SLC6A9 protein, human; D017923:Sodium-Hydrogen Exchangers; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate; D005998:Glycine