In the article by Yu et al. p21-Activated Kinase 4 and Ischemic Acute Kidney Injury in Mice and Humans (J Am Soc Nephrol. 2025;36(7):1264–1277. doi:10.1681/ASN.0000000649), corrections are needed. The authors note that images in Figures 5C and 7C were inadvertently duplicated. The corrected figures appear below.
Figure 5.
Proteasome-dependent degradation of GPx3 by PAK4. (A) HK-2 cells were transfected with PAK4 and either WT or mutant GPx3 and then treated with CHX (30 µg/ml) for 1 or 3 hours. The relative protein levels of GPx3 were compared (n=5). (B) HK-2 cells transfected with hemagglutinin-tagged ubiquitin (HA-Ub) were transfected with WT (GPx3WT) or phospho-deficient GPx3 (GPx3T47A). Cells were exposed to H/R for 12 hours with MG132 (3 µM). Cell lysates were immunoprecipitated with anti-GPx3 antibody followed by immunoblotting with anti-Ub antibody. (C) 8-week-old male Ggt1-Cre KO mice were injected intravenously with WT GPx3 (AAV2-GPx3WT) or GPx3T47A (AAV2-GPx3T47A). After 24-hour reperfusion, I/R-induced tissue injury was determined. Values are mean±SD. 4-HNE, 4-hydroxynonenal; CHX, cycloheximide; Ub, ubiquitin.
Figure 7.
Attenuation of renal I/R injury by PAK4 PROTAC SJ-05. (A) Chemical structure of SJ-05. (B) Schematic diagram of treatment of SJ-05 to C57BL/6 mice. (C) Microscopic pictures of kidney sections and quantification of renal tubular injury (n=4–5). (D) Tertiary complex model of PAK4, CRBN, and the PROTAC SJ-05. The secondary structures of PAK4 and CRBN are colored green and light pink, respectively, with the bound SJ-05 molecule represented as magenta spheres. The lower panel provides a close-up view of the binding interface, illustrating the detailed interactions between SJ-05 and the key residues of PAK4 and CRBN. The key interacting residues are represented in sticks, and H-bonding interactions are depicted with black dashed lines. Hydrogen atoms are undisplayed for visual convenience. Values are mean±SD. PROTAC, proteolysis-targeting chimera; Veh, vehicle; WT, Western blot.
