Differential effect of ik3-1/ Cables  on p53- and p73-induced cell death

doi:10.1074/jbc.M108535200

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Papers In Press, published online ahead of print November 12, 2001
J. Biol. Chem, 10.1074/jbc.M108535200
Submitted on September 5, 2001
Revised on November 2, 2001
Accepted on November 12, 2001

Differential effect of ik3-1/ Cables on p53- and p73-induced cell death

Keitaro Tsuji, Kiyohisa Mizumoto, Tadanori Yamochi, Ikuo Nishimoto, and Masaaki Matsuoka

Department of Pharmacology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582

Corresponding Author: sakimatu{at}med.keio.ac.jp

ik3-1/Cables is associated with cdk3 in self-replicating cells. In postmitotic neurons, it may serve as an adaptor molecule, functionally connecting c-abl and cdk5, and supporting neurite growth. Here we report that ik3-1 binds to p53 and p73 in vivo. Ectopically expressed ik3-1 potentiates p53-induced cell death but not p73-induced cell death in U2OS cells. On the contrary, co-expression of ik3-1-?C, an ik3-1 deletion mutant lacking the C-terminal 134 amino acids (corresponding to the cyclin box-homologous region), inhibits p73-induced cell death but not p53-induced cell death. ik3-1-Å¢C-mediated inhibition of p73-induced cell death are partially attenuated by overexpression of ik3-1. These data indicate that ik3-1 is not only a regulator for p53-induced cell death but also an essential regulator for p73-induced cell death, and ik3-1-?C competes with ik3-1 only in p73-induced cell death. Furthermore, functional domains of p53 responsible for its interaction with ik3-1 are partially different from those of p73. In conclusion, we found that ik3-1, a putative component of cell cycle regulation, is functionally connected with p53 and p73, but in distinct fashions.

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