Mechanisms of cell responses by low dose and low dose-rate irradiation

1.传感器（1）慢性照射通过NO介导的旁观者效应刺激积累的wtp 53的衰减，这表明这种衰减的刺激可能是由于慢性照射激活的Hdm 2降解p53所致。（松本，H.）(2)我们在这里展示了损伤识别的两步机制，其中NBS 1通过与组蛋白H2 AX相互作用来招募Mrel 1核酸酶，然后Mrel 1与受损DNA结合以启动同源重组。（Komatsu，K.）2.（1）低剂量辐射不诱导细胞核信号转导通路，但诱导了希斯顿HB磷酸化的ERK 1/2通路。（Watanabe，M.）(2)在小鼠全身系统的辐射适应性反应中，我们阐明了低剂量窗口和条件照射后的间隔的重要性，作为通过p53肿瘤抑制蛋白的挑战性辐射诱导细胞凋亡的指标。（Ohnishi，T.）3.功能（1）放射敏感性小鼠胸腺淋巴瘤3SB细胞株在电离辐射照射后不久即出现凋亡性细胞死亡，对辐射诱导的凋亡几乎没有剂量率反应。（Suzuki，K）（2）利用鸡DT 40突变体细胞，我们发现低剂量率照射增强细胞存活不是由于HR，而是由于DSB修复的NHEJ修复途径。（内海，H.）(3)基因毒性损伤的完全修复需要两种机制，p53依赖性凋亡组织修复以及众所周知的DNA修复。（Norimura，T.）(4)比较了体细胞和生殖系细胞低剂量辐射诱变的分子本质，发现二者有显著差异。(Ono，T.）(5)照射精子出生的F1小鼠视网膜色素上皮细胞中，母体来源的粉红色眼睛的不稳定等位基因的突变频率升高，表明精子中DNA损伤诱导延迟突变。(Niwa，0.）

1. Sensor(1) Chronic irradiation stimulated the decay of accumulated wtp53 by NO-mediated bystander effect, suggesting that this stimulation of the decay may be due to the degradation of p53 by Hdm2 activated by chronic irradiation. (Matsumoto, H.)(2) We showed here a two-step mechanism for damage recognition, where NBS1 recruits Mrel1 nuclease by interaction to histone H2AX, and then Mrel 1 binds to damaged DNA for initiation of homologous recombination. (Komatsu, K.)2. Signal transaction(1) Low-level radiation did not induce signal translation pathway from nucleolus, but did ERK1/2 pathway for phosholizing histon HB. (Watanabe, M.)(2) In the radioadaptive response of the whole body system in mice, we clarified importance of the window of low dose and the intervals after a conditioning irradiation as an indicator of challenging irradiation-induced apoptosis through a p53 tumor suppressor protein. (Ohnishi, T.)3. Function(1) Radiosensitive mouse thymic lymphoma 3SB cell line exhibited apoptotic cell death shortly after exposure to ionizing radiation and showed little dose rate response to radiation-induced apoptosis. (Suzuki, K)(2) We found that the enhanced cell survival by low-dose rate irradiation owe to not HR but NHEJ repair pathway of DSB repair using the chicken DT40mutant cells. (Utsumi, H.)(3) Complete repair of genotoxic damage requires the two mechanisms, p53-dependent apoptotic tissue repair as well as the well-known DNA repair. (Norimura, T.)(4) Molecular nature of mutants induced by low dose of radiation has been compared between somatic tissues and germ line cells, and a significant difference was observed. (Ono, T.)(5) The frequency of mutation at the maternally derived pink-eyed unstable allele was elevated in the retinal pigment epithelium in Fl mouse born to irradiated sperm, suggesting induction of delayed mutation by DNA damage in sperm. (Niwa, 0.)