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首页> 外文期刊>Radiation Research: Official Organ of the Radiation Research Society >CHARACTERIZATION OF X-RAY-INDUCED IMMUNOSTAINING OF PROLIFERATING CELL NUCLEAR ANTIGEN IN HUMAN DIPLOID FIBROBLASTS
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CHARACTERIZATION OF X-RAY-INDUCED IMMUNOSTAINING OF PROLIFERATING CELL NUCLEAR ANTIGEN IN HUMAN DIPLOID FIBROBLASTS

机译:X射线诱导人二倍体成纤维细胞中增殖细胞核抗原的免疫抑制特性

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The repair of X-ray-induced DNA damage related to the proliferating cell nuclear antigen (PCNA) was characterized in human diploid fibroblasts by an indirect immunofluorescence method. PCNA staining induced by X rays was lost after DNase I treatment but not after RNase treatment. The staining was not induced when ATP was depleted or the temperature was lowered to 0 degrees C during the X irradiation. When cells were incubated at 37 degrees C after X irradiation, PCNA staining diminished gradually and was almost entirely absent 12-15 h later. On the other hand, PCNA staining persisted during aphidicolin treatment even 20 h after X irradiation. Induction of PCNA staining was not affected by the aphidicolin treatment. Cycloheximide treatment did not affect induction of the staining either, but did inhibit the disappearance of the staining. There was no difference in the staining pattern and time course of PCNA staining after X irradiation between normal and xeroderma pigmentosum group A (XP-A) cells. These results imply that PCNA-dependent, aphidicolin-sensitive DNA polymerases may be involved in repair of X-ray-induced DNA damage in vivo, but the repair initiation step could be different from that of nucleotide excision repair initiated by XP proteins. (C) 1996 by Radiation Research Society [References: 39]
机译:通过间接免疫荧光法在人二倍体成纤维细胞中表征了与增殖细胞核抗原(PCNA)相关的X射线诱导的DNA损伤的修复。 X射线诱导的PCNA染色在DNase I处理后消失,但在RNase处理后消失。在X射线照射期间,当ATP耗尽或温度降至0摄氏度时,不会引起染色。 X射线照射后,将细胞在37摄氏度下孵育时,PCNA染色逐渐减少,在12-15小时后几乎完全消失。另一方面,即使在X射线照射后20小时,在蚜虫碱处理期间PCNA染色仍然持续。蚜虫碱处理不影响PCNA染色的诱导。环己二酰亚胺处理也不会影响染色的诱导,但是确实抑制了染色的消失。正常和干性皮肤色素A组(XP-A)细胞在X射线照射后的PCNA染色的染色模式和时间过程上没有差异。这些结果表明,PCNA依赖性,蚜虫敏敏感的DNA聚合酶可能参与体内X射线诱导的DNA损伤的修复,但是修复的起始步骤可能与XP蛋白启动的核苷酸切除修复不同。 (C)1996年,辐射研究学会[参考文献:39]

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