| First Author | Saita Y | Year | 2007 |
| Journal | J Biol Chem | Volume | 282 |
| Issue | 17 | Pages | 12907-15 |
| PubMed ID | 17311925 | Mgi Jnum | J:121272 |
| Mgi Id | MGI:3709707 | Doi | 10.1074/jbc.M611203200 |
| Citation | Saita Y, et al. (2007) Lack of Schnurri-2 expression associates with reduced bone remodeling and osteopenia. J Biol Chem 282(17):12907-15 |
| abstractText | Regulation of bone remodeling determines the levels of bone mass and its imbalance causes major skeletal diseases such as osteoporosis. A zinc finger protein, Schnurri-2 (SHN-2), was recently demonstrated to regulate bone morphogenetic protein-dependent adipogenesis and lymphogenesis. However, the role of SHN-2 in bone is not known. Here, we investigated the effects of Shn-2 deficiency on bone metabolism and cell function in Shn-2-null mice. Lack of SHN-2 expression reduced bone remodeling by suppressing both osteoblastic bone formation and osteoclastic bone resorption activities in vivo. Shn-2 deficiency suppressed osterix and osteocalcin expression as well as in vitro mineralization. Conversely, Shn-2 overexpression enhanced osteocalcin promoter activity and bone morphogenetic protein-dependent osteoblastic differentiation. Shn-2 deficiency suppressed Nfatc1 and c-fos expression leading to reduction of tartrate-resistant acid phosphatase-positive cell development in vivo as well as in the cultures of bone marrow cells. These studies demonstrate that SHN-2 regulates the activities of critical transcription factors required for normal bone remodeling. |
