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The SERCA2b is downregulated but more active due to glutathionylation of the redox-sensitive cysteine

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However, persistently elevated interferons and receptor activation of the MNK1/MNK2eIF4E signaling pathway at all disease phases caused sensorymotor dysfunction and pain by inducing hyperexcitability and sensitization of a GFRA3 + C-fiber subtype of joint-innervating sensory neurons