Impaired interleukin-3 response in Pim-1-deficient bone marrow-derived mast cells
Autor: | J, Domen, N M, van der Lugt, P W, Laird, C J, Saris, A R, Clarke, M L, Hooper, A, Berns |
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Rok vydání: | 1993 |
Předmět: |
Stem Cell Factor
Lymphoid Tissue Immunology Bone Marrow Cells Cell Differentiation Cell Biology Hematology Protein Serine-Threonine Kinases Hematopoietic Cell Growth Factors Biochemistry Mice Mutant Strains Mice Proto-Oncogene Proteins c-pim-1 Proto-Oncogene Proteins hemic and lymphatic diseases Animals Interleukin-3 Mast Cells Cell Division Cells Cultured |
Zdroj: | Blood. 82:1445-1452 |
ISSN: | 1528-0020 0006-4971 |
DOI: | 10.1182/blood.v82.5.1445.bloodjournal8251445 |
Popis: | 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. |
Databáze: | OpenAIRE |
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