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This limitation is partly due to the scarcity of site-specific O-GlcNAc antibodies and methodologies that facilitate site-directed mutagenesis to mimic O-GlcNAc-deficient protein states, in contrast to the well-established resources available for phosphorylation-centric studies

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This study demonstrated that WWP2 was downregulated while p53 was upregulated in ischemia-reperfusion (IR)-induced HK-2 cells