|Title||Impaired interleukin-3 response in Pim-1-deficient bone marrow-derived mast cells.|
|Publication Type||Journal Article|
|Year of Publication||1993|
|Authors||Domen J, van der Lugt NM, Laird PW, Saris C, Clarke AR, Hooper ML, Berns A|
|Date Published||1993 Sep 1|
|Keywords||Animals, Bone Marrow Cells, Cell Differentiation, Cell Division, Cells, Cultured, Hematopoietic Cell Growth Factors, Interleukin-3, Lymphoid Tissue, Mast Cells, Mice, Mice, Mutant Strains, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-pim-1, Stem Cell Factor|
The mouse Pim-1 gene encodes two cytoplasmic serine-threonine-specific protein kinases. The gene has been found to be activated (overexpressed) by retroviral insertion in hematopoietic tumors in mice. Transgenic mice that overexpress Pim-1 (E mu-Pim-1) have a low incidence of spontaneous T-cell lymphomas and an increased susceptibility to Moloney murine leukemia virus and N-ethyl-N-nitrosourea-induced lymphomas. Apart from a slight enlargement of the spleen, no abnormalities were found in prelymphomatous transgenic mice. Inactivation of the Pim-1 gene in the germline of mice resulted in mice with a surprisingly subtle phenotype. Therefore, we investigated whether subtle effects of the absence of Pim-1 could be made visible during in vitro culturing of hematopoietic cells. We found that bone marrow-derived mast cells (BMMC) lacking Pim-1 had a distinct growth disadvantage when grown on interleukin (IL)-3, but not when stimulated by the factors IL-4, IL-9, or Steel factor (SF). This indicates a role for Pim-1 as a modulator of the IL-3 signal transduction pathway.