| First Author | Iotsova V | Year | 1997 |
| Journal | Nat Med | Volume | 3 |
| Issue | 11 | Pages | 1285-9 |
| PubMed ID | 9359707 | Mgi Jnum | J:44112 |
| Mgi Id | MGI:1099363 | Doi | 10.1038/nm1197-1285 |
| Citation | Iotsova V, et al. (1997) Osteopetrosis in mice lacking NF-kappaB1 and NF-kappaB2 [see comments]. Nat Med 3(11):1285-9 |
| abstractText | The nfkb1 and nfkb2 genes encode closely related products regulating immune and inflammatory responses. Their role during development and differentiation remains unclear. The generation of nfkb1 null mice (p50-/-) resulted in altered immune responses, but had no effect on development. Similarly, nfkb2 knockout mice (p52-/-) did not show developmental defects (J.C. et al., manuscript submitted). We have investigated the potential for in vivo compensatory functions of these genes by generating double-knockout mice. The surprising result was that the animals developed osteopetrosis because of a defect in osteoclast differentiation, suggesting redundant functions of NF-kappaB1 and NF-kappaB2 proteins in the development of this cell lineage. The osteopetrotic phenotype was rescued by bone marrow transplantation, indicating that the hematopoietic component was impaired. These results define a new mouse osteopetrotic mutant and implicate NF-kappaB proteins in bone development, raising new directions in the treatment of bone disorders. |
