This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Osteocytes inhibit bone formation by secreting sclerostin, a peptide which is a product of the SOST gene and a negative regulator of osteoblasts (1, 2). Once secreted, sclerostin is transported to the osteoblasts on the bone surface, where it regulates their function. Sclerostin has been shown to inhibit osteoblast development in vitro by inhibiting proliferation, as well as early and late stages of osteoblast differentiation, in both mouse and human osteogenic cells. Sclerostin also stimulates osteoblast apoptosis (3). In sclerosteosis, the inhibitory effect of sclerostin is absent due to mutations in the SOST gene, which results in an increase in bone mass as a result of increased bone formation.
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