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Vol. 13, Issue 10, 3431-3440, October 2002

Radiation-induced Activation of Nuclear Factor-B Involves Selective Degradation of Plasma Membrane-associated IB

Jeffery S. Russell,^* and Philip J. Tofilon

 ^*Department of Experimental Radiation Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030; and  Molecular Radiation Therapeutics Branch, Radiation Oncology Science Program, National Cancer Institute, Bethesda, Maryland 20892

In contrast to nuclear factor-B (NF-B) activation by tumor necrosis factor- (TNF-), the specific processes involved in the activation of this transcription factor by ionizing radiation (IR) have not been completely defined. According to the classical paradigm, a critical event in NF-B activation is the degradation of IB. Data presented herein show that, in contrast to treatment with TNF-, IR-induced NF-B activation was not accompanied by degradation of IB in the U251 glioblastoma cell line as determined in whole cell lysates. However, treatment with the proteosome inhibitor MG-132 inhibited NF-B activation induced by IR, suggesting that IB degradation was a critical event in this process. To reconcile these results, U251 cell lysates were separated into soluble and insoluble fractions and IB levels evaluated. Although IB was found in both subcellular fractions, treatment with IR resulted in the degradation of IB only in the insoluble fraction. Further subcellular fractionation suggested that the IR-sensitive, insoluble pool of IB was associated with the plasma membrane. These data suggest that the subcellular location of IB is a critical determinant in IR-induced NF-B activation.

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Corresponding author. E-mail address: tofilonp{at}mail.nih.gov.

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Molecular Biology of the Cell
Vol. 13, 3431-3440, October 2002
Copyright © 2002 by The American Society for Cell Biology

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