Fig. 10: HK1 stabilizes RANK protein via USP14 mediated de-ubiquitination of RANK in BMDM-derived osteoclasts. | Nature Communications

Fig. 10: HK1 stabilizes RANK protein via USP14 mediated de-ubiquitination of RANK in BMDM-derived osteoclasts.

From: FTO-associated osteoclastogenesis promotes alveolar bone resorption in apical periodontitis male rat via the HK1/USP14/RANK pathway

Fig. 10

a The relative ubiquitination level in OC after treatment with 0.1 mM 2-DG for 4 days was determined by western blotting (n = 3 independent experiments). b The relative protein levels of nuclear factor-κB receptor activator (RANK), nuclear factor of activated T cells (NFATc1), matrix metalloprotein 9 (MMP9), and cathepsin K (CTSK) in 2-DG-treated OC after treatment with MG132 (0.5 μM) were determined by western blotting (n = 3 independent experiments; mean ± SD). c The representative images of RANK (green) and ubiquitin-specific protease 14 (USP14) (red) detection by immunofluorescence in the process of bone marrow macrophage (BMDM)-derived osteoclast (OC). Scale bar indicates 20 μm (n = 3 independent experiments). d Co-IP assay to examine endogenous interaction between USP14 and RANK in BMDM, and BMDM-derived OC at 5 days (n = 3 independent experiments; mean ± SD). e Co-IP assay to examine endogenous USP14 and RANK interaction in HEK-293T cells overexpressing RANK after USP14 and hexokinase 1 (HK1) overexpression for 24 h (n = 3 independent experiments; mean ± SD). The major statistical procedures applied were: Shapro–Wiik test (b, d, e), F-test (b, e), Student-t test (d), Kruskal–Wallis H test and Dunnett-t test (b, e). The statistical test used was two-sided. Source data are available online for this figure.

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