期刊
PLOS ONE
卷 2, 期 9, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0000837
关键词
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资金
- Japanese Ministry of Education, Culture, Sports, Science, and Technology [17390410]
- Terumo Life Science Foundation
- Grants-in-Aid for Scientific Research [17390410] Funding Source: KAKEN
Despite accumulated knowledge of various signalings regulating bone formation, the molecular network has not been clarified sufficiently to lead to clinical application. Here we show that heterozygous glycogen synthase kinase-3 beta (GSK-3 beta)-deficient mice displayed an increased bone formation due to an enhanced transcriptional activity of Runx2 by suppressing the inhibitory phosphorylation at a specific site. The cleidocranial dysplasia in heterozygous Runx2-deficient mice was significantly rescued by the genetic insufficiency of GSK-3 beta or the oral administration of lithium chloride, a selective inhibitor of GSK-3 beta. These results establish GSK-3 beta as a key attenuator of Runx2 activity in bone formation and as a potential molecular target for clinical treatment of bone catabolic disorders like cleidocranial dysplasia.
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