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Radiation induction of immediate early genes: Effectors of the radiation-stress response

https://doi.org/10.1016/0360-3016(94)90539-8Get rights and content

Abstract

Recent studies have demonstrated that the early response genes c-jun, Egr-1, c-fos, and NFKB are induced following exposure of mammalian cells to ionizing radiation. We propose that the products of these early response genes regulate downstream genes that are important in the adaptation of cells and tissues to radiation-induced stress. Potential downstream targets include cytokine and growth factor genes as well as deoxyribonucleic acid (DNA) repair genes. Early response gene products may also regulate cell cycle progression following cellular x-irradiation. Signal transduction pathways that allow cells to adapt to radiation may provide molecular targets to modify tumor and normal responses to radiotherapy.

References (41)

  • C. Cordon-Cardo et al.

    Expression of basic fibroblast growth factor in normal human tissue

    Lab. Invest.

    (1990)
  • R. Datta et al.

    Involvement of reactive oxygen intermediates in the activation of c-jun transcription by ionizing radiation

    Biochemistry

    (1992)
  • R. Datta et al.

    Ionizing radiation activates transcription of the Egr-1 gene via CArG elements

    PNAS

    (1992)
  • Y. DeVary et al.

    Rapid and preferential activation of the c-jun gene during mammalian UV response

    Mol. Cell Biol.

    (1991)
  • A.J. Fornace

    Mammalian genes induced by radiation: Activation of genes associated with growth control

    Ann. Rev. Genet.

    (1992)
  • D. Hallahan et al.

    Radiation signalling mediated by jun activation following dissociations from a cell type specific repressor

    J. Biol. Chem.

    (1993)
  • D.E. Hallahan et al.

    Increased tumor necrosis factor a MRNA production following cellular exposure to ionizing radiation

    PNAS

    (1989)
  • D.E. Hallahan et al.

    Protein kinase mediates x-ray inducibility of nuclear signal transducers Egr-1 and c-jun

    PNAS

    (1991)
  • D.E. Hallahan et al.

    Tumor necrosis factor gene expression mediated by protein kinase c activation by ionizing radiation

    Cancer Res.

    (1991)
  • A. Haimovitz-Friedman et al.

    Autocrine effects of fibroblast growth factors in radiation damage repair in human endothelial cells

    Cancer Res.

    (1991)
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    Presented at the 1993 ASTR.O Meeting, New Orleans, LA.

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