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The Journal of Neuroscience, September 17, 2008, 28(38):9404-9413; doi:10.1523/JNEUROSCI.3351-08.2008

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Cellular/Molecular
A Dominant Role of GTRAP3-18 in Neuronal Glutathione Synthesis

Masahiko Watabe, * Koji Aoyama, * and Toshio Nakaki

Department of Pharmacology, Teikyo University School of Medicine, Tokyo 173-8605, Japan

Correspondence should be addressed to Toshio Nakaki, Department of Pharmacology, Teikyo University School of Medicine, 2-11-1, Kaga, Itabashi-ku, Tokyo 173-8605, Japan. Email: nakaki{at}med.teikyo-u.ac.jp

Glutathione is an essential reductant which protects cells and is reduced in neurodegenerative disorders such as Parkinson's and Alzheimer's diseases. Neurons rely mainly on extracellular cysteine for glutathione synthesis and a cysteine transporter termed excitatory amino acid carrier 1 (EAAC1). However, the mechanisms underlying neuronal cysteine uptake have remained elusive. Herein, we show glutamate transport-associated protein for EAAC1 (GTRAP3-18) to interact with EAAC1 at the plasma membrane and thereby regulate neuronal glutathione levels. Glutathione increased in the mouse brain as well as in primary cultured neurons, when the GTRAP3-18 protein level was decreased by genetic manipulations, whereas glutathione decreased when GTRAP3-18 was increased. Furthermore, glutathione contents that had been increased, by a translocator and activator of EAAC1, were suppressed by increased cell surface GTRAP3-18 protein. Our results demonstrate GTRAP3-18 to dominantly and negatively determine the intracellular glutathione contents in neurons.

Key words: glutathione; oxidative stress; neuroprotection; neuron; transporter; neurodegeneration

Received Nov. 10, 2007; accepted Aug. 8, 2008.

Correspondence should be addressed to Toshio Nakaki, Department of Pharmacology, Teikyo University School of Medicine, 2-11-1, Kaga, Itabashi-ku, Tokyo 173-8605, Japan. Email: nakaki{at}med.teikyo-u.ac.jp




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