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机构地区:[1]南京医科大学第一附属医院皮肤科,210029
出 处:《国际皮肤性病学杂志》2009年第1期27-29,共3页International Journal of Dermatology and Venereology
基 金:基金项目:国家自然科学基金(30771946)
摘 要:研究发现,端粒降解是引发DNA损伤反应的起始事件,这一起始事件的实质可能是原本隐藏的端粒单链3’端悬突结构遭到暴露。而外源性端粒同源寡核苷酸能在无紫外线诱导的DNA损伤发生的情况下模拟这个端粒降解信号,并提高机体DNA损伤修复的能力以抵抗紫外线辐射造成的损伤。端粒同源寡核苷酸引发SOS反应并导致恶性转化细胞发生选择性凋亡的特点为光源性皮肤肿瘤的防治提供一种新方法。Telomere degradation is reported to be the initial event that triggers multiple DNA damage responses, and the nature of the event is likely to be the disclosure of concealed single-stranded 3' overhang. Exogenous telomere homolog oligonucleotide can mimic the signal of telomere degradation in the absence of UV-induced DNA damage, and enhance the DNA repair capacity of organisms, so as to defend against the damage induced by UV irradiation. The fact that telomere homolog oligonucleotides trigger SOS-like responses and cause selective apoptosis of malignantly transformed cells may provide an important clue to the prevention and treatment of photo-induced skin tumors.
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