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Superior cervical ganglion-10 protein as a molecular effector of c-Jun N-terminal kinase 1: implications for the therapeutic targeting of Jun N-terminal kinase in nerve regeneration

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Tumor necrosis factor-α-induced sickness behavior is impaired by central administration of an inhibitor of c-jun N-terminal kinase

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Hydrogen peroxide inhibits the immune response to lipopolysaccharide by attenuating signaling through c-Jun N-terminal kinase and p38 associated with protein kinase C

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c-Jun N-terminal kinases as potential therapeutic targets

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