Sokolova I A, Cowan K H, Schneider E
Medicine Branch, National Cancer Institute, Bethesda, MD 20892, USA.
Biochim Biophys Acta. 1995 Apr 28;1266(2):135-42. doi: 10.1016/0167-4889(94)00233-5.
Apoptosis is now recognized as one of the major processes regulating the size of cell populations. However, despite intensive investigations the biochemical and enzymological mechanisms involved in apoptosis remain unclear. In the present study we demonstrate activation of a Ca2+/Mg(2+)-dependent endonuclease during VP-16-induced apoptosis in MCF7 cells. Nuclease activation occurred prior to the appearance of internucleosomal DNA fragmentation, suggesting that this activation may be an early and possibly critical step in drug-induced apoptosis. Analysis of the internucleosomal DNA fragments showed that they contained phosphorylated 5'-ends, indicating that they were produced by a Ca2+/Mg(2+)-dependent endonuclease.
细胞凋亡现在被认为是调节细胞群体大小的主要过程之一。然而，尽管进行了深入研究，参与细胞凋亡的生化和酶学机制仍不清楚。在本研究中，我们证明了在VP-16诱导的MCF7细胞凋亡过程中，一种Ca2+/Mg(2+)依赖性核酸内切酶被激活。核酸酶激活发生在核小体间DNA片段化出现之前，这表明这种激活可能是药物诱导细胞凋亡的早期且可能是关键步骤。对核小体间DNA片段的分析表明，它们含有磷酸化的5'末端，这表明它们是由Ca2+/Mg(2+)依赖性核酸内切酶产生的。
