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. 2021 Jan 18;12:426. doi: 10.1038/s41467-020-20677-0

Fig. 5. PKC activation during diabetes causes MOR degradation in lumbar DRG.

Fig. 5

a Kinase activity assay to compare PKC activation in the lumbar DRG of control and diabetic mice (n = 8 mice/group, 1–2 replicates from each mouse; two-tailed t-test; ***p < 0.0001). b Lumbar DRG protein lysates from control and diabetic mice (n = 3 each) pooled and immunoprecipitated(IP) using MOR-specific antibody (UMB3) and immunoblotted(IB) using pan-phosphothreonine antibody to determine phosphorylation of MOR. c In vitro, primary DRG neurons transfected with MOR-mCherry construct and exposed to normal glucose (NG, 17 mM) or HG (high glucose, 40 mM) in the presence or absence of a PKC inhibitor (Gö6983, 1 μM, 48 h). Surface association of MOR assessed by overlap of WGA-stained cell membrane and mCherry signal (n = total of 11–15 images analyzed from 3 independent experiments; one-way ANOVA followed by Tukey’s post-hoc test; ***p < 0.0001). d Typical examples showing co-immunostaining of control and diabetic lumbar DRG sections with a MOR-specific antibody and lysosomal marker (Lamp1) (n = 6 mice/group, 3–6 DRG sections from each mouse). For all panels, female mice data are shown; data represent mean ± SEM; with 95% C.I. Scale = 20 μm. Circles represent individual data points. Source data are provided as a Source Data file.