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Publication : TRAF5 functions in both RANKL- and TNFalpha-induced osteoclastogenesis.

First Author  Kanazawa K Year  2003
Journal  J Bone Miner Res Volume  18
Issue  3 Pages  443-50
PubMed ID  12619928 Mgi Jnum  J:111298
Mgi Id  MGI:3653569 Doi  10.1359/jbmr.2003.18.3.443
Citation  Kanazawa K, et al. (2003) TRAF5 functions in both RANKL- and TNFalpha-induced osteoclastogenesis. J Bone Miner Res 18(3):443-50
abstractText  Although TRAF6 is essential for both RANKL- and TNFalpha-induced osteoclastogenesis, it has remained unclear whether other members of the TRAF family are involved in osteoclastogenesis. We examined TRAF5 function in both RANKL- and TNFalpha-induced osteoclastogenesis by using osteoclast progenitor cells from TRAF5-deficient mice. The results demonstrated that RANKL or TNFalpha did not effectively induce osteoclast differentiation from osteoclast progenitor cells derived from these mice into mature multinucleated osteoclasts, although c-jun N-terminal kinase (JNK) and NF-kappaB activation was apparently observed in osteoclast progenitor cells. In the parathyroid hormone (PTH)-induced hypercalcemia model, calcium concentration peaked at day 3 after administration. However, in TRAF5-deficient mice, this peak was delayed and found at day 5, showing less effective osteoclast differentiation. Thus, we have provided the first evidence showing that TRAF5 is involved in osteoclastogenesis.
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