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Inactivation of DNA-dependent protein kinase by protein kinase Cdelta: implications for apoptosis

A Bharti1, S K Kraeft, M Gounder

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

Insights

Protein kinase Cdelta (PKCdelta) activation during apoptosis involves its interaction with DNA-dependent protein kinase (DNA-PK). This interaction inhibits DNA-PK, suggesting a role in DNA damage-induced cell death.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Protein kinase Cdelta (PKCdelta) is activated during apoptosis induced by various stimuli, including DNA damage.
  • Overexpression of the active PKCdelta catalytic fragment (PKCdelta CF) mimics apoptotic features, but its precise role remains unclear.

Purpose of the Study:

  • To elucidate the functional relationship between PKCdelta activation and the induction of apoptosis.
  • To investigate the molecular interactions of PKCdelta during DNA damage-induced apoptosis.

Main Methods:

  • Investigated the association between PKCdelta and DNA-dependent protein kinase catalytic subunit (DNA-PKcs).
  • Assessed the phosphorylation of DNA-PKcs by PKCdelta CF in vitro.
  • Evaluated the impact of PKCdelta CF on DNA-PKcs function and complex formation with DNA.
  • Examined apoptosis induction in DNA-PK deficient cells overexpressing PKCdelta CF.

Main Results:

  • PKCdelta constitutively associates with DNA-PKcs.
  • PKCdelta CF phosphorylates DNA-PKcs, inhibiting its DNA binding and p53 phosphorylation.
  • Cells lacking DNA-PK are resistant to apoptosis induced by PKCdelta CF overexpression.

Conclusions:

  • Functional interactions between PKCdelta and DNA-PKcs are crucial for DNA damage-induced apoptosis.
  • PKCdelta-mediated inhibition of DNA-PKcs contributes to the apoptotic process.

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