Lee S, Elenbaas B, Levine A, Griffith J
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill 27599-7295, USA.
Cell. 1995 Jun 30;81(7):1013-20. doi: 10.1016/s0092-8674(05)80006-6.
Insertion/deletion (IDL) mismatches in DNA are lesions consisting of extra bases on one strand. Here, the binding of p53 and its 14 kDa C-terminal domain to DNAs containing one or three 3-cytosine IDL mismatches was examined. Electron microscopy showed that both p53 forms bound predominantly as tetramers at the lesions while single-stranded binding proteins did not bind. Gel retardation assays showed that p53 formed highly stable complexes when the DNA contained the IDL mismatches, but only unstable complexes when the DNA lacked lesions (but did contain free ends). The highly stable complexes had a half-life of > 2 hr, suggesting that upon encountering lesions, p53 may recruit other proteins to the site, providing a signal for DNA damage.
DNA中的插入/缺失（IDL）错配是由一条链上额外碱基组成的损伤。在此，研究了p53及其14 kDa C末端结构域与含有一个或三个3-胞嘧啶IDL错配的DNA的结合情况。电子显微镜显示，两种p53形式主要以四聚体形式结合在损伤部位，而单链结合蛋白不结合。凝胶阻滞分析表明，当DNA含有IDL错配时，p53形成高度稳定的复合物，但当DNA没有损伤（但确实含有游离末端）时，只形成不稳定的复合物。高度稳定的复合物半衰期大于2小时，这表明遇到损伤时，p53可能会将其他蛋白质招募到该部位，为DNA损伤提供信号。
