Kristupaitis D, Dibirdik I, Vassilev A, Mahajan S, Kurosaki T, Chu A, Tuel-Ahlgren L, Tuong D, Pond D, Luben R, Uckun F M
Biotherapy Program, University of Minnesota, Minneapolis, Minnesota 55455, USA.
J Biol Chem. 1998 May 15;273(20):12397-401. doi: 10.1074/jbc.273.20.12397.
Here we present evidence that exposure of DT40 lymphoma B-cells to low energy electromagnetic fields (EMF) results in activation of phospholipase C-gamma 2 (PLC-gamma2), leading to increased inositol phospholipid turnover. PLC-gamma2 activation in EMF-stimulated cells is mediated by stimulation of the Bruton's tyrosine kinase (BTK), a member of the Src-related TEC family of protein tyrosine kinases, which acts downstream of LYN kinase and upstream of PLC-gamma2. B-cells rendered BTK-deficient by targeted disruption of the btk gene did not show enhanced PLC-gamma2 activation in response to EMF exposure. Introduction of the wild-type (but not a kinase domain mutant) human btk gene into BTK-deficient B-cells restored their EMF responsiveness. Thus, BTK exerts a pivotal and mandatory function in initiation of EMF-induced signaling cascades in B-cells.
在此，我们提供证据表明，将DT40淋巴瘤B细胞暴露于低能量电磁场（EMF）会导致磷脂酶C-γ2（PLC-γ2）激活，进而导致肌醇磷脂周转率增加。EMF刺激细胞中PLC-γ2的激活是由布鲁顿酪氨酸激酶（BTK）的刺激介导的，BTK是Src相关的TEC家族蛋白酪氨酸激酶的成员，其作用于LYN激酶下游和PLC-γ2上游。通过靶向破坏btk基因而使BTK缺乏的B细胞在暴露于EMF时未显示出增强的PLC-γ2激活。将野生型（而非激酶结构域突变体）人btk基因导入BTK缺乏的B细胞可恢复其对EMF的反应性。因此，BTK在启动B细胞中EMF诱导的信号级联反应中发挥关键和必需的作用。
