Abstract
Abstract: 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.
Dates
Type | When |
---|---|
Created | 15 years, 1 month ago (July 15, 2010, 4:06 p.m.) |
Deposited | 1 year, 10 months ago (Oct. 26, 2023, 7:44 p.m.) |
Indexed | 1 month, 3 weeks ago (July 7, 2025, 1:45 a.m.) |
Issued | 29 years, 10 months ago (Nov. 1, 1995) |
Published | 29 years, 10 months ago (Nov. 1, 1995) |
Published Online | 22 years, 9 months ago (Nov. 23, 2002) |
Published Print | 29 years, 10 months ago (Nov. 1, 1995) |
@article{Sato_1995, title={Modulation of a Recombinant Glycine Transporter (GLYT1b) by Activation of Protein Kinase C}, volume={65}, ISSN={1471-4159}, url={http://dx.doi.org/10.1046/j.1471-4159.1995.65051967.x}, DOI={10.1046/j.1471-4159.1995.65051967.x}, number={5}, journal={Journal of Neurochemistry}, publisher={Wiley}, author={Sato, Kohji and Adams, Ralf and Betz, Heinrich and Schloss, Patrick}, year={1995}, month=nov, pages={1967–1973} }