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M512128200v1
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Papers In Press, published online ahead of print December 12, 2005
J. Biol. Chem, 10.1074/jbc.M512128200
Submitted on November 10, 2005
Accepted on December 12, 2005

The RASSF1A tumor suppressor activates Bax via MOAP-1

Michele D. Vos, Ashraf Dallol, Kristen Eckfeld, Nadia P. C. Allen, Howard Donninger, Luke B. Hesson, Diego Calvisi, Farida Latif, and Geoffrey J. Clark

Cell and Cancer Biology, NCI, Rockville, MD 20850-3300

Corresponding Author: gclark{at}mail.nih.gov

The novel tumor suppressor RASSF1A is frequently inactivated during human tumorigenesis by promoter methylation. RASSF1A may serve as a node in the integration of signaling pathways controlling a range of critical cellular functions including cell cycle, genomic instability, and apoptosis. The mechanism of action of RASSF1A remains under investigation. We now identify a novel pathway connecting RASSF1A to Bax via the Bax binding protein MOAP-1. RASSF1A and MOAP-1 interact directly and this interaction is enhanced by the presence of activated K-Ras. RASSF1A can activate Bax via MOAP-1. Moreover, activated K-Ras, RASSF1A and MOAP-1 synergize to induce Bax activation and cell death. Analysis of a tumor-derived point mutant of RASSF1A showed that the mutant was defective for the MOAP-1 interaction and for Bax activation. Moreover, inhibition of RASSF1A by shRNA impaired the ability of K-Ras to activate Bax. Thus, we identify a novel pro-apoptotic pathway linking K-Ras, RASSF1A and Bax that is specifically impaired in some human tumors.


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