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J. Biol. Chem., Vol. 277, Issue 4, 2951-2957, January 25, 2002

This Article Full Text Full Text (PDF) An addition or correction has been published All Versions of this Article: 277/4/2951    most recent M108535200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tsuji, K. Articles by Matsuoka, M. Search for Related Content PubMed PubMed Citation Articles by Tsuji, K. Articles by Matsuoka, M. Social Bookmarking                      What's this?

Differential Effect of ik3-1/Cables on p53- and p73-induced Cell Death^*

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

From the  Department of Pharmacology, KEIO University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan and the ^§ Department of Biochemistry, School of Pharmaceutical Sciences, Kitasato University, Shirokane, Minato-ku, Tokyo 108-8641, Japan

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, coexpression 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-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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