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J Biol Chem, Vol. 273, Issue 20, 12397-12401, May 15, 1998

Electromagnetic Field-induced Stimulation of Bruton's Tyrosine Kinase

Daiva Kristupaitis, Ilker Dibirdik^§, Alexei Vassilev^§, Sandeep Mahajan^§, Tomohiro Kurosaki^¶, Alice Chu^§, Lisa Tuel-Ahlgren^§, Dong Tuong^§, David Pond^§, Richard Luben, and Fatih M. Uckun^§

From the  Biotherapy Program, University of Minnesota, Minneapolis, Minnesota 55455, the  Division of Biomedical Sciences, University of California, Riverside, California 92521, the ^§ Wayne Hughes Institute, St. Paul, Minnesota 55113, and the ^¶ Department of Molecular Genetics, Kansai Medical University, Institute for Hepatic Research, Moriguchi, Osaka 570, Japan

Here we present evidence that exposure of DT40 lymphoma B-cells to low energy electromagnetic fields (EMF) results in activation of phospholipase C- 2 (PLC-2), leading to increased inositol phospholipid turnover. PLC-2 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-2. B-cells rendered BTK-deficient by targeted disruption of the btk gene did not show enhanced PLC-2 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.

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