Defective induction of stress-activated protein kinase activity in ataxia-telangiectasia cells exposed to ionizing radiation.
Defective induction of stress-activated protein kinase activity in ataxia-telangiectasia cells exposed to ionizing radiation.
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暴露于电离辐射的共济失调毛细血管扩张细胞中应激激活蛋白激酶活性的诱导缺陷。
作者：
T. Shafman;A. Saleem;J. Kyriakis;R. Weichselbaum;S. Kharbanda;D. Kufe
应激激活蛋白(SAP)激酶的活性受到多种药物的刺激，如肿瘤坏死因子、紫外线和蛋白质合成抑制剂。目前的研究表明，电离辐射(IR)暴露也与SAP激酶活性的诱导有关。来自共济失调-毛细血管扩张症(A-T)患者的细胞具有对IR超敏的特点。在这项研究中，我们证明了IR诱导的A-T细胞SAP激酶的激活是有缺陷的。相反，A-T细胞暴露于紫外光或山奈霉素会导致SAP激酶活性的诱导。这些发现表明，在A-T细胞中，参与SAP激酶激活的IR诱导信号是有缺陷的。
The activity of stress-activated protein (SAP) kinase is stimulated by diverse agents such as tumor necrosis factor, UV light, and protein synthesis inhibitors. The present study demonstrates that ionizing radiation (IR) exposure is also associated with the induction of SAP kinase activity. Cells derived from patients with ataxia-telangiectasia (A-T) are characterized by hypersensitivity to IR. In this study, we demonstrate that IR-induced activation of SAP kinase is defective in A-T cells. In contrast, exposure of A-T cells to UV light or anisomycin results in the induction of SAP kinase activity. These findings indicate that IR-induced signals involved in SAP kinase activation are defective in A-T cells.
DOI：
10.1073/pnas.87.15.5663
发表时间：
1990-08
影响因子：
11.1
作者：
M. Sherman;R. Datta;D. Hallahan;R. Weichselbaum;D. Kufe
通讯作者：
M. Sherman;R. Datta;D. Hallahan;R. Weichselbaum;D. Kufe
正常、共济失调性毛细血管扩张和遗传性视网膜母细胞瘤成纤维细胞中 X 射线诱导的细胞杀伤动力学的比较。
DOI：
10.1016/0027-5107(83)90054-4
发表时间：
1983
期刊：
Mutation research
影响因子：
--
作者：
Nagasawa,H;Little,JB
通讯作者：
Little,JB