| First Author | Nicola NA | Year | 1996 |
| Journal | Blood | Volume | 87 |
| Issue | 7 | Pages | 2665-74 |
| PubMed ID | 8639882 | Mgi Jnum | J:32978 |
| Mgi Id | MGI:80466 | Doi | 10.1182/blood.v87.7.2665.bloodjournal8772665 |
| Citation | Nicola NA, et al. (1996) Functional inactivation in mice of the gene for the interleukin-3 (IL-3)-specific receptor beta-chain: implications for IL-3 function and the mechanism of receptor transmodulation in hematopoietic cells. Blood 87(7):2665-74 |
| abstractText | The receptors for granulocyte-macrophage colony- stimulating factor (GM-CSF) and interleukin-3 and -5 (IL- 3, IL-5) share a common signaling subunit (beta c). However, in the mouse, IL-3 can also use an alternative IL- 3-specific receptor beta-chain (beta IL-3). To assess the relative contributions of beta c and beta IL-3 to IL-3 receptor formation and function, mice were generated in which the beta IL-3 gene was functionally inactivated by replacement of exons 9-13 with a neomycin resistance cassette. Bone marrow cells from these mice displayed a lower affinity IL-3 receptor than normal and were hyporesponsive to IL-3, but the mice displayed no obvious hematopoietic abnormalities. The data suggested that beta c and beta IL-3 are normally coexpressed on IL-3- responsive cells and have identical qualitative signaling capacities. Receptor transmodulation studies on bone marrow cells from wild-type, beta c-/-, and beta IL-3-/- mice showed that the previously described hierarchical pattern of transmodulation was dependent on the relative numbers of both beta IL-3 and beta c receptor chains and also provided evidence for an unexpected interaction between beta c chains and G-CSF and M-CSF receptors. (C) 1996 by The American Society of Hematology. |
