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. Author manuscript; available in PMC: 2023 Jan 19.
Published in final edited form as: J Bone Miner Res. 2016 Sep 26;32(2):385–396. doi: 10.1002/jbmr.2986

Fig. 3.

Fig. 3.

Aberrant NFATc1 activation and RANKL-mediated osteoclastogenesis in TRPML1−/− mice. BMMs isolated from WT and TRPML1−/− mice were cultured and used for the experiments below. (A) RANKL-mediated NFATc1 expression is suppressed in TRPML1−/− BMMs. β-actin was used as a loading control. (B) Deletion of TRPML1 reduces RANKL-mediated MNC formation. The number of TRAP-positive MNCs, which are identified by the presence of more than 3 nuclei and cell size larger than 100 μm in diameter, present in each well were counted. The columns are the mean±SD of 5 experiments. (Scale bar = 100 μm). (C) Deletion of TRPML1 alters expression of differentiation marker genes for RANKL-mediated osteoclastogenesis. Results are presented as fold increase compared to WT cells treated with DW. *p < 0.05, **p < 0.01.

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