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A more recent version of this article appeared on October 1, 2002
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Submitted on May 2, 2002
Revised on July 3, 2002
Accepted on July 10, 2002
B involves the selective degradation of plasma membrane-associated IB
1 Department of Experimental Radiation Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030; and the Molecular Radiation Therapeutics Branch, Radiation Oncology Science Program, National Cancer Institute, Bethesda, MD 20892
2 Molecular Radiation Therapeutics Branch, Radiation Oncology Science Program, National Cancer Institute, Bethesda, MD 20892
* Corresponding author. E-mail address: tofilonp{at}mail.nih.gov.
In contrast to NF-B activation by 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 here 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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