Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 287, Issue 42, Pages 35057-35064Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M111.328930
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Funding
- Ministry of Education, Science, and Culture
- Uehara Memorial Foundation
- Nakatomi Foundation
- Mochida Memorial Foundation
- Grants-in-Aid for Scientific Research [23791626, 24119505, 23659868] Funding Source: KAKEN
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Osteoclast differentiation is one of the critical steps that control bone mass levels in osteoporosis, but the molecules involved in osteoclastogenesis are still incompletely understood. Here, we show that two-pore channel 2 (TPC2) is expressed in osteoclast precursor cells, and its knockdown (TPC2-KD) in these cells suppressed RANKL-induced key events including multi-nucleation, enhancement of tartrate-resistant acid phosphatase (TRAP) activities, and TRAP mRNA expression levels. With respect to intracellular signaling, TPC2-KD reduced the levels of the RANKL-induced dynamic waving of Ca2+ in RAW cells. The search for the target of TPC2 identified that nuclear localization of NFATc1 is retarded in TPC2-KD cells. Finally, TPC2-KD suppressed osteoclastic pit formation in cultures. We conclude that TPC2 is a novel critical molecule for osteoclastogenesis.
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