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Function for p300 and not CBP in the apoptotic response to DNA damage

Z M Yuan1, Y Huang, T Ishiko

  • 1Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, MA 02115, USA.

Oncogene
|October 19, 1999
PubMed

Insights

p300 protein, not CBP, is crucial for cellular response to DNA damage and ionizing radiation-induced apoptosis. Cells lacking p300 show impaired DNA damage response and reduced sensitivity to radiation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Ionizing radiation (IR) triggers cellular apoptosis.
  • p300 and CBP are transcriptional coactivators with histone acetyltransferase activity.
  • Their roles in DNA damage response are not fully defined.

Purpose of the Study:

  • To investigate the specific roles of p300 and CBP in cellular response to DNA damage.
  • To determine the contribution of p300 and CBP to IR sensitivity and apoptosis.

Main Methods:

  • Generation of cells deficient in p300 or CBP.
  • Assessment of cellular sensitivity to ionizing radiation.
  • Analysis of IR-induced apoptosis in deficient cell lines.

Main Results:

  • p300 deficiency, but not CBP deficiency, increases cellular sensitivity to IR.
  • IR-induced apoptosis is significantly impaired in p300-deficient cells.
  • CBP-deficient cells do not exhibit impaired apoptosis following IR exposure.

Conclusions:

  • p300 plays a critical role in mediating the apoptotic response to DNA damage induced by IR.
  • p300 is essential for IR-induced apoptosis, while CBP's role in this specific context is less significant.

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