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Fig. 8 | Molecular Medicine

Fig. 8

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

Fig. 8

The schematic diagram representing the current working model in our study. In brief, BCL2 phosphorylation at Ser87 can dissociate the BCL2-BAX complex, subsequently making proapoptotic molecule BAX lead to apoptotic signal transduction and promote apoptosis, which is not conducive to the differentiation of OCPs into mature osteoclasts. BCL2 phosphorylation at Ser70 can dissociate the BCL2-Beclin1 complex, enabling autophagic molecule Beclin1 to enter autophagic flux and activate autophagy, which represses apoptosis and is conducive to osteoclastic differentiation. RANKL is a stimulator of BCL2 phosphorylation at Ser70, but not Ser87. Therefore, RANKL can induce osteoclastogenesis by phosphorylating BCL2 at Ser70. P phosphorylation, OCP osteoclast precursor, OC osteoclast

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Molecular Medicine

ISSN: 1528-3658