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Interaction of c-Abl and p73α and their collaboration to induce apoptosis

Author

Listed:
  • Reuven Agami

    (The Weizmann Institute of Science)

  • Giovanni Blandino

    (The Weizmann Institute of Science)

  • Moshe Oren

    (The Weizmann Institute of Science)

  • Yosef Shaul

    (The Weizmann Institute of Science)

Abstract

c-Abl, a non-receptor tyrosine kinase, is activated by agents that damage DNA. This activation results in either arrest of the cell cycle in phase G1 or apoptotic cell death, both of which are dependent on the kinase activity of c-Abl1. p73, a member of the p53 family of tumour-suppressor proteins2,3, can also induce apoptosis3. Here we show that the apoptotic activity of p73α requires the presence of functional, kinase-competent c-Abl. Furthermore, p73 and c-Abl can associate with each other, and this binding is mediated by a PxxP motif in p73 and the SH3 domain of c-Abl. We find that p73 is a substrate of the c-Abl kinase and that the ability of c-Abl tophosphorylate p73 is markedly increased by γ-irradiation. Moreover, p73 is phosphorylated in vivo in response to ionizing radiation. These findings define a pro-apoptotic signalling pathway involving p73 and c-Abl.

Suggested Citation

  • Reuven Agami & Giovanni Blandino & Moshe Oren & Yosef Shaul, 1999. "Interaction of c-Abl and p73α and their collaboration to induce apoptosis," Nature, Nature, vol. 399(6738), pages 809-813, June.
    • Handle: RePEc:nat:nature:v:399:y:1999:i:6738:d:10.1038_21697
    DOI: 10.1038/21697
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