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Fig. 1 | Molecular Medicine

Fig. 1

From: Phosphorylation of BCL2 at the Ser70 site mediates RANKL-induced osteoclast precursor autophagy and osteoclastogenesis

Fig. 1

RANKL promoted BCL2 phosphorylation at S70, not S87, in OCPs. A OCPs were treated with the indicated concentration of RANKL for 30 min in α-MEM with 1% FBS (appropriate starvation for enhancing the phosphorylation effect). Phosphorylated BCL2 at S70, i.e., p-BCL2 (S70), and phosphorylated BCL2 at S87, i.e., p-BCL2 (S87), were detected using western blotting assays. B Dynamic changes in p-BCL2 (S70) and p-BCL2 (S87) in OCPs. The protein expression level was normalized to that of the control samples (5 ng/mL). C OCPs were treated with or without 100 ng/mL RANKL for the indicated times in α-MEM with 1% FBS. p-BCL2 (S70) and p-BCL2 (S87) were detected using western blotting assays. D, E Dynamic changes in p-BCL2 (S70) and p-BCL2 (S87) in OCPs. The protein expression level was normalized to that of the control samples (0 min). At different time points, pairwise comparisons were made between the RANKL group and the control group. The experiments were replicated at least three times. Data are presented as the mean ± SEM from three independent experiments. ***P < 0.001, **P < 0.01. ns not significant, Cont the control group without RANKL intervention

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