First Author | Neubauer H | Year | 1998 |
Journal | Cell | Volume | 93 |
Issue | 3 | Pages | 397-409 |
PubMed ID | 9590174 | Mgi Jnum | J:47298 |
Mgi Id | MGI:1203273 | Doi | 10.1016/s0092-8674(00)81168-x |
Citation | Neubauer H, et al. (1998) Jak2 deficiency defines an essential developmental checkpoint in definitive hematopoiesis. Cell 93(3):397-409 |
abstractText | Janus kinases (Jaks) play an important role in signal transduction via cytokine and growth factor receptors. A targeted inactivation of Jak2 was performed. Jak2-/- embryos are anemic and die around day 12.5 postcoitum. Primitive erythrocytes are found, but definitive erythropoiesis is absent. Compared to erythropoietin receptor-deficient mice, the phenotype of Jak2 deficiency is more severe. Fetal liver BFU-E and CFU-E colonies are completely absent. However, multilineage hematopoietic stem cells (CD34low, c-kit(pos)) can be found, and B lymphopoiesis appears intact. In contrast to IFNalpha stimulation, Jak2- /- cells do not respond to IFNgamma. Jak2-/- embryonic stem cells are competent for LIF signaling. The data provided demonstrate that Jak2 has pivotal functions for signal transduction of a set of cytokine receptors required in definitive erythropoiesis. |