Effect of the insulin-like growth factor I receptor on ionizing radiation-induced cell death in mouse embryo fibroblasts.
Effect of the insulin-like growth factor I receptor on ionizing radiation-induced cell death in mouse embryo fibroblasts.
复制标题
胰岛素样生长因子 I 受体对小鼠胚胎成纤维细胞电离辐射诱导的细胞死亡的影响。
DOI：
--
复制
发表时间：
1997
影响因子：
3.7
通讯作者：
Takehito Sasaki
中科院分区：
文献类型：
--
作者：
Shin Nakamura;Hiroshi Watanabe;M. Miura;Takehito Sasaki
我们使用以下两种小鼠胚胎成纤维细胞系研究了胰岛素样生长因子 I 受体 (IGF-IR) 对电离辐射 (IR) 诱导的细胞死亡的影响：(i) IGF-IR 基因无效突变的 R-细胞，因此不表达内源性 IGF-IR； (ii)源自R-细胞的R+细胞，R-细胞是过表达人IGF-IR的稳定转染子。在 10 Gy 的 X 射线照射后约 48 小时，大量 R 细胞开始从培养皿中脱离并漂浮到培养基中。通过琼脂糖凝胶电泳检测到的核小体间 DNA 断裂是细胞凋亡的特征，在漂浮的 R 细胞中观察到，但在贴壁细胞中未观察到。出乎意料的是，照射72小时后对漂浮细胞的形态学分析显示，只有大约一半的细胞表现出凋亡性死亡，其余的则表现出非凋亡，可能是坏死的。另一方面，R+细胞在照射后4天仍保持90%以上的活力，并且观察到很少的漂浮细胞。照射后，两种细胞系均诱导 G2 停滞，并且 G2/M 分数在照射后约 20 小时类似地恢复到正常水平，表明此后在 R 细胞中出现的细胞死亡是通过有丝分裂介导的。在 R- 或 R+ 细胞中，通过蛋白质印迹分析未检测到辐射后 p53 的显着诱导。总的来说，这些结果表明源自 IGF-IR 的信号转导途径可能参与预防 IR 诱导的细胞凋亡和坏死，而不影响细胞周期停滞或 p53 途径。
We have investigated the effect of the insulin-like growth factor I receptor (IGF-IR) on ionizing radiation (IR)-induced cell death using the following two mouse embryo fibroblast cell lines: (i) R- cells with a null mutation of the IGF-IR gene, therefore expressing no endogenous IGF-IR; (ii) R+ cells derived from R- cells, a stable transfectant overexpressing the human IGF-IR. Numbers of R- cells began to detach from dishes and float into the medium about 48 h after 10 Gy of X-irradiation. Internucleosomal DNA fragmentation detected by agarose gel electrophoresis, which is characteristic of apoptosis, was observed in the floating R- cells, but not in the attached cells. Unexpectedly, morphological analysis of the floating cells 72 h after irradiation revealed that only about half of them showed apoptotic death and the rest showed a nonapoptotic, presumably necrotic, one. On the other hand, R+ cells retained more than 90% viability even 4 days after irradiation, and very few floating cells were observed. The G2 arrest was induced in both cell lines following irradiation and G2/M fractions similarly returned to normal levels by around 20 h after irradiation, indicating that the cell death which appeared thereafter in R- cells is mediated through mitosis. Significant induction of p53 following irradiation was not detected by Western blot analysis in either R- or R+ cells. Collectively, these results demonstrate that signal transduction pathways originating from the IGF-IR may be involved in preventing IR-induced apoptosis and necrosis without affecting cell cycle arrest or p53 pathways.
登录
查看更多内容
影响因子：
4.8
作者：
M. G. Myers;X. Sun;B. Cheatham;BOZENA R. Jachna;Erin Glasheen;J. Backer;M. White
通讯作者：
M. G. Myers;X. Sun;B. Cheatham;BOZENA R. Jachna;Erin Glasheen;J. Backer;M. White
胰岛素样生长因子 I 受体酪氨酸 950 突变对细胞生长和转化的影响。
DOI：
--
发表时间：
1995
期刊：
Cancer research.
影响因子：
--
作者：
Miura,M;Li,S;Baserga,R
通讯作者：
Baserga,R
影响因子：
8
作者：
C. Guillouf;Filippo Rosselli;K. Krishnaraju;E. Moustacchi;B. Hoffman;D. Liebermann
通讯作者：
C. Guillouf;Filippo Rosselli;K. Krishnaraju;E. Moustacchi;B. Hoffman;D. Liebermann
v-myc 癌基因与 H-ras 对放射抗性的协同作用。
影响因子：
11.2
作者：
McKenna,WG;Weiss,MC;Endlich,B;Ling,CC;Bakanauskas,VJ;Kelsten,ML;Muschel,RJ
通讯作者：
Muschel,RJ
DOI：
10.1073/pnas.90.23.11217
发表时间：
1993-12-01
影响因子：
11.1
作者：
SELL, C;RUBINI, M;BASERGA, R
通讯作者：
BASERGA, R