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Fig. 8 Overview of wfs1b Deficiency-Mediated ER Stress Inhibits M-cell Axon Regeneration. The wfs1b knockout impeded the M-cell axon regeneration due to increased ER stress, resulting in up-regulated mRNA expression of the UPR pathway. The ER stress activator TM inhibited M-cell axon regeneration in wfs1b+/+ zebrafish larvae, whereas both the application of ER stress inhibitor 4-PBA and complementation of wfs1b at the single-cell level ameliorated the degenerated M-cell axon in wfs1b−/− zebrafish larvae
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Full text @ Acta Neuropathol Commun