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Recognition of Abasic Sites in DNA by a Cyclobisacridine Molecule

机译:Cyclobisacridine分子对DNA中无碱基位点的识别

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The ability of the cyclobisacridine CBA to recognize the abasic lesion in DNA was investigated with modified synthetic oligonucleotide duplexes. CBA was shown to cleave a ~(32)P-labeled duplex oligomer (23-mer) containing an apurinic site in the middle of the sequence. The interaction was examined with duplex which contain a stable tetrahydrofuranyl analogue at the abasic site. Thermal denaturation experiments showed that CBA stabilizes an abasic undecamer duplex by a #DELTA#T_m value of 14 deg C by forming a 1:1 complex, while no interaction was detected with the unmodified parent duplex. CBA displaced a nitroxide abasic site specific probe from the abasic duplex. When irradiated in the presence of a ~(32)P-labeled model abasic site containing duplex (23-mer), CBA induced selective photocleavage in the vicinity of the abasic lesion on both strands. All results demonstrate the high specificity of the interaction of CBA at the abasic lesion.
机译:用修饰的合成寡核苷酸双链体研究了环双ac啶CBA识别DNA中无碱基病变的能力。已显示CBA裂解〜(32)P标记的双链寡聚物(23-mer),在序列中间包含一个嘌呤位点。用在无碱基位置含有稳定的四氢呋喃基类似物的双链体检查相互作用。热变性实验表明,CBA通过形成1:1配合物,通过14摄氏度的#DELTA#T_m值来稳定无碱基的十聚体双链体,而未检测到与未修饰的亲本双链体的相互作用。 CBA从无碱基双链体置换了氮氧化物无碱基位点特异性探针。当在〜(32)P标记的含双链体(23-mer)的模型无碱基位点的存在下进行辐照时,CBA在两条链的无碱基病变附近诱导选择性光裂解。所有结果表明,CBA在无基础病变处的相互作用具有很高的特异性。

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