IL‐4 activates a distinct signal transduction cascade from IL‐3 in factor‐dependent myeloid cells.
IL‐4 activates a distinct signal transduction cascade from IL‐3 in factor‐dependent myeloid cells.
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IL-4 在因子依赖性骨髓细胞中激活与 IL-3 不同的信号转导级联。
DOI：
10.1002/j.1460-2075.1992.tb05596.x
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发表时间：
1992
期刊：
影响因子：
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通讯作者：
Jacalyn H. Pierce
中科院分区：
文献类型：
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作者：
Ling;A. Keegan;William E. Paul;M. Heidaran;J. Gutkind;Jacalyn H. Pierce
白细胞介素4(IL-4)对依赖IL-3的髓系祖细胞株FDCP-2有明显的促有丝分裂反应。尽管IL-4不能维持FDCP-2细胞的长期生长，但它能促进FDCP-2细胞在含有IL-3的无血清介质中的生长。IL-4能显著激活迁移到170 kDa的底物(S)的酪氨酸磷酸化，而对包括IL-4受体在内的其他几种蛋白的磷酸化作用不明显。相反，IL-3诱导同一细胞系中145、97、70、55和52 kDa的蛋白质发生不同的酪氨酸磷酸化。IL-4处理FDCP-2细胞后，磷脂酰肌醇3-激酶(PI-3-Kinase)与170 kDa酪氨酸磷酸化底物和IL-4受体本身都有很强的结合。相反，IL-3仅触发PI3-激酶活性与97 kDa底物的微弱关联。虽然IL-4不影响细胞RAF，但IL-3刺激确实引起其流动性的变化，推测是由于丝氨酸/苏氨酸的磷酸化。综上所述，我们的结果表明，IL-4和IL-3在相同的细胞背景下激活了不同的磷酸化级联反应；这可能反映了这两种细胞因子生物学功能的不同。
Interleukin‐4 (IL‐4) was shown to induce a potent mitogenic response in the IL‐3‐dependent myeloid progenitor cell line, FDCP‐2. Although IL‐4 could not sustain long‐term growth of FDCP‐2 cells, it enhanced their growth in serum‐free medium containing IL‐3. IL‐4 triggered prominent tyrosine phosphorylation of a substrate(s) migrating at 170 kDa and less striking phosphorylation of several other proteins, including the IL‐4 receptor. By contrast, IL‐3 induced distinct tyrosine phosphorylation of proteins migrating at 145, 97, 70, 55 and 52 kDa in the same cell line. IL‐4 treatment of FDCP‐2 cells caused a dramatically strong association of phosphatidylinositol 3‐kinase (PI 3‐kinase) both with the 170 kDa tyrosine phosphorylated substrate and with the IL‐4 receptor itself. By contrast, IL‐3 triggered only weak association of PI 3‐kinase activity with the 97 kDa substrate. While IL‐4 did not affect cellular raf, IL‐3 stimulation did induce a shift in its mobility presumably due to serine/threonine phosphorylation. Taken together, our results indicate that IL‐4 and IL‐3 activate distinct phosphorylation cascades in the same cell background; this may reflect a difference in the biological function of these two cytokines.