P53 mutations in human cancer.
P53 mutations in human cancer.
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作者：
C. Miller;Koeffler Hp
1987年，一种名为p53的53,000道尔顿蛋白被发现在人类癌症中发生突变。进一步的研究表明，p53是一种肿瘤抑制基因，可能是所有类型癌症中最常见的改变基因之一。这些改变包括与病毒抗原的相互作用、编码突变和使重排失活。越来越多的证据表明p53通过结合DNA和激活转录来起作用。p53的表达与组成启动子转染后，阻断细胞增殖和导致凋亡细胞死亡。在正常细胞中，照射诱导p53表达；这导致了p53在基因修复过程中抑制复制的假设。缺乏p53的细胞更容易产生扩增。缺乏p53的小鼠出生时正常，但在几个月后发展为癌症，这表明p53不是癌症的初始突变，而可能是一个晚期事件。
A 53,000 dalton protein called p53, was noted to be mutated in human cancer in 1987. Further studies have shown that p53 is a tumor suppressor gene which may be one of the most frequently altered genes in cancer of all types. These alterations include interactions with viral antigens, coding mutations and inactivating rearrangements. Accumulating evidence suggests that p53 acts by binding DNA and activating transcription. Expression of p53 after transfection with a constitutive promotor, blocks cellular proliferation and leads to an apoptotic cell death. In normal cells, p53 expression is induced by irradiation; this has led to the hypothesis that p53 acts to inhibit replication during genetic repair. Cells which lack p53 are more prone to develop amplification. Mice lacking p53 are born normal but develop cancer after a lag of months, this suggests that p53 is not an initiating mutation in cancer, but probably a late event.