Uckun F M, Kurosaki T, Jin J, Jun X, Morgan A, Takata M, Bolen J, Luben R
Department of Therapeutic Radiology-Radiation Oncology, University of Minnesota Health Sciences Center, Minneapolis 55455, USA.
J Biol Chem. 1995 Nov 17;270(46):27666-70. doi: 10.1074/jbc.270.46.27666.
Here, we present evidence that exposure of B-lineage lymphoid cells to low energy electromagnetic fields (EMF) stimulates the protein tyrosine kinases Lyn and Syk, results in tyrosine phosphorylation of multiple electrophoretically distinct substrates, and leads to downstream activation of protein kinase C (PKC). EMF exposure enhances protein tyrosine phosphorylation in Syk deficient but not in Lyn-deficient B-lineage lymphoid cells and stimulates Lyn kinase activity in wild-type as well as Syk-deficient B-lineage lymphoid cells. These results indicate that activation of Lyn kinase is sufficient and mandatory for EMF-induced tyrosine phosphorylation in B-lineage lymphoid cells. The PKC activity increases later than the Lyn activity and pretreatment with the PTK inhibitors genistein or herbimycin A abrogates the EMF-induced PKC signal. Thus, stimulation of Lyn is a proximal and mandatory step in EMF-induced activation of PKC in B-lineage lymphoid cells. Our observations prompt the hypothesis that a delicate growth regulatory balance might be altered in B-lineage lymphoid cells by EMF-induced activation of Lyn.
在此,我们提供证据表明,B 系淋巴样细胞暴露于低能量电磁场(EMF)会刺激蛋白酪氨酸激酶 Lyn 和 Syk,导致多种电泳性质不同的底物发生酪氨酸磷酸化,并引发蛋白激酶 C(PKC)的下游激活。EMF 暴露增强了 Syk 缺陷型而非 Lyn 缺陷型 B 系淋巴样细胞中的蛋白酪氨酸磷酸化,并刺激野生型以及 Syk 缺陷型 B 系淋巴样细胞中的 Lyn 激酶活性。这些结果表明,Lyn 激酶的激活对于 B 系淋巴样细胞中 EMF 诱导的酪氨酸磷酸化而言是充分且必要的。PKC 活性的增加晚于 Lyn 活性,并且用蛋白酪氨酸激酶(PTK)抑制剂染料木黄酮或赫曲霉素 A 进行预处理可消除 EMF 诱导的 PKC 信号。因此,Lyn 的刺激是 B 系淋巴样细胞中 EMF 诱导的 PKC 激活的近端且必要步骤。我们的观察结果促使我们提出这样一个假设,即 EMF 诱导的 Lyn 激活可能会改变 B 系淋巴样细胞中微妙的生长调节平衡。