Interleukin-4-dependent proliferation dissociates p44erk-1, p42erk-2, and p21ras activation from cell growth.

作者: M.J. Welham , V. Duronio , J.W. Schrader

DOI: 10.1016/S0021-9258(17)37541-5

关键词:

摘要: The activation of erk/mitogen-activated protein kinases and p21ras is strongly associated with progression through the cell cycle. Cell growth induced by cytokine interleukin-4 (IL-4) effectively dissociates p44erk-1 p42erk-2 mitogen-activated from proliferation. In two lines T lymphocyte myeloid origin that were dependent upon IL-4 for continuous growth, failed to detectably activate or induce tyrosine phosphorylation p42erk-2. was also not affected treatment these cells. Treatment same cells other factors (colony-stimulating factor-1 Steel factor) phorbol esters stimulated activity. presence neither diminished nor enhanced colony-stimulating factor-1, factor, 12-O-tetradecanoylphorbol-13-acetate. Furthermore, p44erk-1, p42erk-2, in normal lymphocytes mast derived spleen bone marrow, respectively. Significantly, findings demonstrate IL-4-induced may be dissociated p21ras, suggesting their an absolute requirement factor-stimulated mitogenesis.

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