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Further in vivo studies indicated that P

AMR1, an arabidopsis gene that coordinately and negatively regulates the mannose/L-galactose ascorbic acid biosynthetic pathway

CD8 + T cells, activated by APCs via MHC class I molecules, differentiate into cytotoxic T lymphocytes (CTLs), which eliminate pathogen-infected or tumor cells through the release of perforin and granzymes [34, 35]

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The data robustly suggest that despite its role in reducing the ERs GSHpool, CHAC1 does not influence the UPR, implying that GSHdepletion alone may not be sufficient to disrupt protein folding homeostasis to a degree that activates the UPR