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Molecular mechanisms and clinical implications of reversible protein S-glutathionylation

In summary, according to the model presented here, ME/CFS develops in three steps: first, an acquired EBV immunodeficiency develops in individuals with weak HLA-II haplotypes against EBV, which prevents control of latency I cells

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In analyses of ChIP-seq data, we observed that many of these genes were devoid of NRF2 in their promoter regions

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