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The Asp-glutamate transporter SLC1A3 is closely associated with the effect of ETC inhibitors, and the SLC1A3 site is amplified in subclusters of non-glial epithelial tumors and thus against aspartic restriction

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AtGLR3.4 mediates Ca 2+ influx during osmotic stress, and cold or glutamate treatments activate these channels, which are blocked by antagonists such as DNQX and CNQX (Meyerhoff et al