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			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
			C.

			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
			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.

			PMID: 7595479 [Indexed for MEDLINE]

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