PubMed Journals: J Neurochem
Source: PMID: 7595479
⇦ ⇨ J Neurochem. 1995 Nov;65(5):1967-73.
Modulation of a recombinant glycine transporter
(GLYT1b) by activation of protein kinase
Sato K(1), Adams R, Betz H, Schloss P.
(1) Abteilung Neurochemie, Max-Planck-Institut
für Hirnforschung, Frankfurt, Germany.
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
(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.
PMID: 7595479 [Indexed for MEDLINE]