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Publication : Inhibition of erythropoietin-induced mitogenesis by a kinase-deficient form of Jak2.

First Author  Zhuang H Year  1994
Journal  J Biol Chem Volume  269
Issue  34 Pages  21411-4
PubMed ID  8063772 Mgi Jnum  J:19924
Mgi Id  MGI:68043 Doi  10.1016/s0021-9258(17)31818-5
Citation  Zhuang H, et al. (1994) Inhibition of erythropoietin-induced mitogenesis by a kinase-deficient form of Jak2. J Biol Chem 269(34):21411-4
abstractText  Receptors for a variety of hematopoietins, interferons alpha/beta and gamma, and growth hormone have recently been shown to mediate rapid, ligand-dependent activation of the Janus-type cytosolic protein-tyrosine kinases Jak1, Jak2, and/or tyk-2. This finding extends relatedness among class I and II cytokine receptors to a functional context and provides an initially satisfying mechanistic analogy to protein-tyrosine kinase-encoding receptors of the epidermal growth factor/platelet-derived growth factor/insulin family. Through the construction and expression of a kinase-deficient form of Jak2 (JK2 delta VIII) in interleukin-3 (IL-3)/erythropoietin (Epo)-dependent DAER cells, we have tested whether activation of Jak2 is required for induced mitogenesis via these class I cytokine receptors. Ectopic expression of JK2 delta VIII inhibited Epo- and IL-3-induced activation of endogenous wild-type Jak2, transiently attenuated IL-3-dependent growth, and essentially abrogated Epo-induced proliferation in this model system. These dominant-negative effects provide the first direct experimental evidence for an essential role for Janus kinase activation in mitogenesis and suggest that distinct effectors may mediate IL-3-induced versus Epo-induced pathways.
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