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In a similar manner, genetic deletion of the excitatory amino acid carrier type 1 (EAAC1), a glutamate transporter which also participates in the neuronal uptake of cysteine for GSH synthesis, significantly sensitized mice to TBI induced by controlled cortical impact, resulting in enhanced neuronal death and increased microglial activation (Aoyama et al., 2006

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This process is crucial for preventing the degradation of replication-dependent (RD) histone mRNAs and ensuring an adequate histone supply

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