@misc{oai:repo.qst.go.jp:00062521,
 author = {Vares, Guillaume and Bing, Wang and Nenoi, Mitsuru and Tanaka, Kaoru and Hayata, Isamu and Ｇｕｉｌｌａｕｍｅ Ｖａｒｅｓ and 王 冰 and 根井 充 and 田中 薫 and 早田 勇},
 month = {Nov},
 note = {Exposure of sublethal doses of ionizing radiation can induce protective mechanisms against a subsequent higher dose irradiation. We demonstrated the existence of this phenomenon, called adaptive response (AR), in mice during late organogenesis. Molecular mechanisms underlying AR in this model were investigated. Using DNA microarrays, AR-specific gene modulations were identified. Our results suggested the involvement of signal transduction and p53-related pathways in the induction of AR. In order to validate microarray results and to gain better insights into molecular mechanisms of AR in fetal mice, we analyzed the expression kinetics of several target genes by real-time quantitative fluorescence RT-PCR in different organs of irradiated embryos. Whole-body expression of Csf1 gene was significantly different after exposure to AR-inducing and non AR-inducing priming radiation. Comparative gene expression in adapted and non-adapted fetuses will be presented. In an in vitro model of cultured limb bud cells from mouse fetuses, we checked p53 protein expression and phosphorylation levels on Ser18 following priming and challenging irradiations. After exposure to challenging dose alone or to 0.5 Gy priming dose (not efficient for inducing AR) before challenging radiation, p53 protein expression and phosphorylation, initially at low levels, peaked 4 to 6h after exposure to challenge dose. When priming dose was performed in AR-inducing conditions, these values followed similar time course, but reached lower peak level. The involvement of p53 protein in AR in this model will be discussed., New Nuclear Research Symposium "Biological Responses to Low Dose Radiation"},
 title = {Adaptive response in mice during late embyogenesis: gene modulations and role of p53},
 year = {2007}
}