期刊
DEVELOPMENTAL CELL
卷 14, 期 6, 页码 914-925出版社
CELL PRESS
DOI: 10.1016/j.devcel.2008.03.022
关键词
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资金
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R37AR046523, R01AR032788, R01AR046852, R21AR054190, R01AR046523] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM064625] Funding Source: NIH RePORTER
- NIAMS NIH HHS [R21 AR054190, AR054190, AR046852, R21 AR054190-02, R01 AR046852-09, R01 AR032788-23, AR032788, R01 AR046523-10, R01 AR032788, R01 AR046852, AR046523, R37 AR046523, R01 AR046523] Funding Source: Medline
- NIGMS NIH HHS [R01 GM064625] Funding Source: Medline
Maintenance of bone mass and integrity requires a tight balance between resorption by osteoclasts and formation by osteoblasts. Exocytosis of functional proteins is a prerequisite for the activity of both cells. In the present study, we show that synaptotagmin VII, a calcium sensor protein that regulates exocytosis, is associated with lysosomes in osteoclasts and bone matrix protein-containing vesicles in osteoblasts. Absence of synaptotagmin VII inhibits cathepsin K secretion and formation of the ruffled border in osteoclasts and bone matrix protein deposition in osteoblasts, without affecting the differentiation of either cell. Reflecting these in vitro findings, synaptotagmin VII-deficient mice are osteopenic due to impaired bone resorption and formation. Therefore, synaptotagmin VII plays an important role in bone remodeling and homeostasis by modulating secretory pathways functionally important in osteoclasts and osteoblasts.
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