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| Reports on Overseas' Conferences and Meetings |
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Reports on the 2nd Asian Congress of
Radiation Research (ACRR 2009) |
| Masatoshi Suzuki, Department of Molecular Medicine |
ACRR2009 was held from May 18th to 20th in Seoul, Korea. According to an announcement by organizing committee, more than five hundred researchers from 13 countries participated to this meeting. Many topics from molecular biology to translational research on radiation research were discussed in this meeting.
One of my interesting presentations was about RASSF1A function on p53 stabilization in response to DNA-damage presented by Dr. Lim from Korea. In general, it is thought that p53 is usually ubiquitinated by MDM2 and degraded through proteasome-system. What they found was that MDM2 self-ubiquitination was regulated by the association with RASSF1A in response to DNA-damage and this interaction influenced p53 stabilization through p53 ubiquitination status. MDM2, which is regulated by self-ubiquitination of MDM2, forms the complex with DAXX/ HAUSP, deubiquitinase, however, RASSF1A was replaced into the MDM2/DAXX complex instead of HAUSP in response to DNA-damage and MDM2 was highly ubiquitinated and was degraded. Consequently p53 was stabilized by loss of the interaction with MDM2.
Since p53 is a key molecule to induce stress-induced premature senescence, SIPS, that was described in my presentation, the mechanism of p53 stabilization they proposed stimulated me to elucidate the further mechanism of SIPS-induction. Overall, a major idea in this meeting was still pointed out the efficient induction of apoptosis to improve radiation therapy, however our data and others in the poster session clearly showed that not only apoptosis but also non-apoptotic cell death, in which SIPS is involved, was induced in tumor cells exposed to ionizing radiation, suggesting the induction of non-apoptotic cell death could be also applicable to efficient radiotherapy in addition to the induction of apoptosis.
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The venue: COEXj |
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