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. 2020 Dec 12;70(10):1872–1883. doi: 10.1136/gutjnl-2020-322468

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© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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DSS-mediated NF-κB-p65 subunit/IKKβ O-GlcNAcylation and subsequent NF-κB signalling activation in mouse were alleviated by BtGH84 and AkkGH84. Mice were treated with control, DSS, DSS+BtGH84, DSS+AkkGH84, DSS+BtGH84-2D and DSS+AkkGH84-2D as described in methods. (A, C, D) Colonic tissue lysates were immunoprecipitated with anti-NF-κB-p65 or anti-IKKβ antibody. The O-GlcNAcylated NF-κB-p65 and IKKβ were detected using anti-O-GlcNAc antibody. (B, E, F) Cytosolic and nuclear sections from colonic tissue lysates were analysed by immunoblots for IκBα and NF-κB-p65, respectively. β-actin serves as a loading control of cytosolic section; histone-H3 serves as a loading control of nuclear. Data represent the mean of 3 repeats per group with the SD; *P<0.05, **P<0.01, ***P<0.001. DSS, dextran sulfate sodium; NS, not significant.