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BER Research Highlights


Publication from Low Dose Radiation Research Program Highlighted on Cover of Cancer Research
Published: January 01, 2007
Posted: January 17, 2007

Important new work from LBNL scientist Dr. Mary Helen Barcellos-Hoff demonstrates a previously unsuspected role for extracellular signaling by TGF-beta1 protein in the cellular response to DNA damage induced by ionizing radiation. The research, funded by both DOE and NASA, is testing the revolutionary idea that extracellular signaling controls DNA damage response. DNA damage elicits a cellular response program of damage control coordinated by the kinase activity of the ATM protein. Kirshner, et al., show that ATM activity, but not its abundance, is severely compromised in mouse cells in which the TGF-beta1 gene is deleted and in human epithelial cells in which TGF-beta1 signaling is blocked by an inhibitor. As a consequence of the failure of ATM to phosphorylate its substrates, cells exhibit increased radiosensitivity, as demonstrated by compromised radiation-induced apoptosis and cell-cycle arrest, and by increased cell kill measured in clonogenic assays. Future studies to identify the molecular mechanisms of TGF-beta1 protein inhibition may support the use of these inhibitors to increase response to radiotherapy. For details, see the cover article in the November 15, 2006, issue of Cancer Research, beginning on page 10861.

Contact: Noelle Metting, SC-23.2, (301) 903-8309
Topic Areas:

  • Legacy: Low Dose Radiation, Radiobiology
  • Legacy: Medical Applications

Division: SC-33.2 Biological Systems Science Division, BER
      (formerly SC-23.2 Medical Sciences Division, OBER)

 

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