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. Author manuscript; available in PMC: 2024 Jan 27.
Published in final edited form as: J Med Chem. 2023 Apr 7;66(8):5657–5668. doi: 10.1021/acs.jmedchem.2c02089

Figure 6. JSD26 treatment increases S-nitrosylation of PKM2 and inhibits PKM2 activity.

Figure 6.

(A) S-nitrosylation of PKM2 in sham-surgery or I/R-injured kidneys from DMSO-treated or JSD26-treated mice. Three mice per group are all shown. Samples processed without ascorbate (−Ascorbate) is a negative control for SNO. Input is used as loading control. (B) Quantification of SNO-PKM2. SNO-PKM2 is normalized to input PKM2 (n=3 per group). (C) Activity of endogenous pyruvate kinase (PK) in sham-surgery or I/R-injured kidneys from DMSO-treated or JSD26-treated mice; (n=4 per group) Uninjured (sham) kidney expresses PKM1 that is insensitive to S-nitrosylation, while AKI kidney expresses mainly PKM2.9 All results are presented as mean ± SD. One-way ANOVA with Tukey post hoc was used to detect significance. *, p<0.05.