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Modulation of a Recombinant Glycine Transporter (GLYT1b) by Activation of Protein Kinase C
Author(s) -
Sato Kohji,
Adams Ralf,
Betz Heinrich,
Schloss Patrick
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.65051967.x
Subject(s) - protein kinase c , staurosporine , activator (genetics) , phosphorylation , phorbol , microbiology and biotechnology , chemistry , biochemistry , biology , receptor
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 [ 3 H]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.