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Mechanistically, oxidative stress triggers endoplasmic reticulum stress through the activation of the PERK-eIF2-ATF4 and IRE1-XBP1 signaling pathways, as well as through the upregulation of CHOP (C/EBP homologous protein), which promotes apoptotic signaling (75) as shown in Figure 4

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To confirm these results, we knockeddown unc1 expression in a tissuespecific manner using RNAi by expressing doublestranded RNAs against the gene across the entire nervous system ( rab3 promoter) using transgenesis (Appendix Fig S8)

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We report here a multi-omics analysis in patients with ME/CFS and healthy controls (HC), before and 24 h after exercise, that suggests models for understanding the pathogenesis of chronic inflammation, fatigue, and PEM in ME/CFS