Physiological Functions of Osteoblast Lineage and T Cell–Derived RANKL in Bone Homeostasis
Version of Record online: 19 MAR 2014
© 2014 American Society for Bone and Mineral Research
Journal of Bone and Mineral Research
Volume 29, Issue 4, pages 830–842, April 2014
How to Cite
Fumoto, T., Takeshita, S., Ito, M. and Ikeda, K. (2014), Physiological Functions of Osteoblast Lineage and T Cell–Derived RANKL in Bone Homeostasis. J Bone Miner Res, 29: 830–842. doi: 10.1002/jbmr.2096
- Issue online: 19 MAR 2014
- Version of Record online: 19 MAR 2014
- Accepted manuscript online: 7 SEP 2013 04:51AM EST
- Manuscript Accepted: 31 AUG 2013
- Manuscript Revised: 25 JUL 2013
- Manuscript Received: 1 APR 2013
- JSPS KAKENHI for Scientific Research B. Grant Number: 22390064
- JSPS KAKENHI for Young Investigator. Grant Number: 21790374
- MEXT KAKENHI for Scientific Research on Innovative Areas. Grant Number: 22118007
- Promotion of Fundamental Studies in Health Sciences program of the National Institute of Biomedical Innovation (NIBIO) of Japan. Grant Number: 06-31
- Longevity Sciences from the Ministry of Health, Labor, and Welfare of Japan. Grant Number: H23-12
Additional Supporting Information may be found in the online version of this article.
Figure S1. Generation and confirmation of a floxed Rankl allele.
Figure S2. Bone phenotype of mice with T cell–specific inactivation of Rankl.
Figure S3. Mice with osteoblast lineage–specific deficiency of RANKL are partially protected from osteoclastogenesis in K/B×N model.
Figure S4. Mice with T cell–specific deficiency of RANKL are not protected from the development of RA.
Figure S5. Gene expression in osteoblast- and osteocyte-rich fractions.
Table S1. Oligonucleotide primers for qPCR.
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