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.

			Author Information
			(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]

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