| First Author | Betz UA | Year | 1998 |
| Journal | J Exp Med | Volume | 188 |
| Issue | 10 | Pages | 1955-65 |
| PubMed ID | 9815272 | Mgi Jnum | J:67677 |
| Mgi Id | MGI:1931128 | Doi | 10.1084/jem.188.10.1955 |
| Citation | Betz UA, et al. (1998) Postnatally induced inactivation of gp130 in mice results in neurological, cardiac, hematopoietic, immunological, hepatic, and pulmonary defects. J Exp Med 188(10):1955-65 |
| abstractText | The pleiotrophic but overlapping functions of the cytokine family that includes interleukin (IL)-6, IL-11, leukemia inhibitory factor, oncostatin M, ciliary neurotrophic factor, and cardiotrophin 1 are mediated by the cytokine receptor subunit gp130 as the common signal transducer. Although mice lacking individual members of this family display only mild phenotypes, animals lacking gp130 are not viable. To assess the collective role of this cytokine family, we inducibly inactivated gp130 via Cre-loxP-mediated recombination in vivo. Such conditional mutant mice exhibited neurological, cardiac, hematopoietic, immunological, hepatic, and pulmonary defects, demonstrating the widespread importance of gp130-dependent cytokines. |
