Peptide nucleic acids (PNAs): potential antisense and anti-gene agents.
Peptide nucleic acids (PNAs): potential antisense and anti-gene agents.
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肽核酸（PNA）：潜在的反义和反基因剂。
DOI：
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发表时间：
1993
期刊：
影响因子：
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通讯作者：
Ole Buchardt
中科院分区：
文献类型：
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作者：
Peter E. Nielsen;M. Egholm;Rolf Henrik Berg;Ole Buchardt
利用核酸酶S1探针研究了肽核酸（PNAs） T10-LysNH2、T5CT4-LysNH2和T2CT2CT4-LysNH2与双链DNA靶点A10、A5GA4和A2GA2GA4的结合。研究发现，PNAs优先与互补靶标结合，对含有一个错配的靶标较弱，而对含有两个错配的靶标则不强。利用RNA聚合酶T3体外转录系统，发现启动子下游结合的PNA T10-LysNH2仅当PNA与模板链结合时，才会在PNA结合位点引起转录延伸阻滞。最后，研究表明Taq DNA聚合酶在单链模板上的引物延伸在占用的PNA T10结合位点被阻止。这些结果与PNAs作为潜在的反义和抗基因药物有关。
The binding of peptide nucleic acids (PNAs) T10-LysNH2, T5CT4-LysNH2 and T2CT2CT4-LysNH2 to double-stranded DNA targets A10, A5GA4 and A2GA2GA4 was studied by nuclease S1 probing. It is found that the PNAs bind preferentially to their complementary targets, weaker to targets containing one mismatch and not to targets containing two mismatches. Using an RNA polymerase T3 in vitro transcription system, it is found that a PNA T10-LysNH2 bound downstream from the promoter causes transcription elongation arrest at the PNA binding site only when the PNA is bound to the template strand. Finally, it is shown that primer extension by Taq DNA polymerase on a single-stranded template is arrested at an occupied PNA T10 binding site. These results are discussed in relation to PNAs as potential anti-sense and anti-gene drugs.