| First Author | Bouvard D | Year | 2007 |
| Journal | Development | Volume | 134 |
| Issue | 14 | Pages | 2615-25 |
| PubMed ID | 17567669 | Mgi Jnum | J:122741 |
| Mgi Id | MGI:3715389 | Doi | 10.1242/dev.000877 |
| Citation | Bouvard D, et al. (2007) Defective osteoblast function in ICAP-1-deficient mice. Development 134(14):2615-25 |
| abstractText | The integrin receptor family plays important roles in cell-to-cell and cell-to-extracellular matrix interactions through the recruitment of accessory molecules. One of them, the integrin cytoplasmic domain-associated protein-1 (ICAP-1; also known as ITGB1BP1), specifically interacts with the cytoplasmic domain of the beta(1) integrin subunit and negatively regulates its function in vitro. To address the role of ICAP-1 in vivo, we ablated the Icap-1 gene in mice. We report an unexpected role of ICAP-1 in osteoblast function during bone development. Icap-1-deficient mice suffer from reduced osteoblast proliferation and delayed bone mineralization, resulting in the retarded formation of bone sutures. In vitro studies reveal that primary and immortalized Icap-1-null osteoblasts display enhanced adhesion and spreading on extracellular matrix substrates, probably owing to an increase in beta(1) integrin activation. Finally, we provide evidence that ICAP-1 promotes differentiation of osteoprogenitors by supporting their condensation through modulating the integrin high affinity state. |
