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Science 26 May 2006:
Vol. 312. no. 5777, p. 1101
DOI: 10.1126/science.312.5777.1101k
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This Week in Science
Adult bone mass is determined by the rates of bone formation by osteoblasts and bone resorption by osteoclasts. Genetic mutations that disrupt the function of these cells can lead to problems with skeletal development, including excessive postnatal bone formation. Pivotal in osteoblast differentiation is the transcriptional regulator Runx2. Jones et al. (p. 1223) reveal how this master control protein is itself regulated. Mice lacking the adapter protein Schnurri-3 accumulated bone mass because of increased osteoblast activity resulting from abnormal Runx2 turnover within the cell. Runx2 is normally regulated by ubiquitin-mediated degradation through the Schnurri-3-dependent association with the E3 ubiquitin ligase WWP1. The identification of this upstream pathway regulating postnatal bone formation might help reveal therapeutic avenues for treating bone abnormalities and deficiencies, such as osteoporosis.
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Science. ISSN 0036-8075 (print), 1095-9203 (online)
