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. 2022 Nov;17(11):2427-2428.
doi: 10.4103/1673-5374.335806.

Targeting O-GlcNAcylation in ischemic stroke

Xuan Li  1 , Wei Yang  1
Affiliations

Targeting O-GlcNAcylation in ischemic stroke

Xuan Li et al. Neural Regen Res. 2022 Nov.
No abstract available

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Figures

Figure 1
Figure 1
The XBP1s/HBP/O-GlcNAc axis. Activated IRE1 splices Xbp1 mRNA, which is then translated into XBP1s protein. XBP1s, a transcriptional factor, can upregulate the expression of HBP enzymes, including GFAT (*, the rate-limiting enzyme of HBP). The HBP produces UDP-GlcNAc, which is the sugar donor for O-GlcNAcylation, a post-translational modification. Glucosamine and thiamet-G have been used to pharmacologically increase O-GlcNAcylation. ER: Endoplasmic reticulum; GFAT: glutamine fructose-6-phosphate aminotransferase; GNK: GlcNAc kinase; GNPNAT1: glucosamine-phosphate N-acetyltransferase 1; HBP: hexosamine biosynthetic pathway; IRE1: inositol-requiring enzyme 1; OGA: O-GlcNAcase; OGT: O-GlcNAc transferase; PGM3: phosphoglucomutase 3; UDP-GlcNAc: uridine diphosphate N-acetylglucosamine.
See this image and copyright information in PMC

References

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