Department of Medical Genetics, University of Alberta, Edmonton, Alberta, Canada.
DNA Repair (Amst). 2010 Feb 4;9(2):161-8. doi: 10.1016/j.dnarep.2009.11.010.
Many studies have shown that DNA mismatch repair (MMR) has a role beyond that of repair in response to several types of DNA damage, including ultraviolet radiation (UV). We have demonstrated previously that the MMR-dependent component of UVB-induced apoptosis is integral to the suppression of UVB-induced tumorigenesis. Here we demonstrate that Msh6-dependent UVB-induced apoptotic pathway is both activated via the mitochondria and p53-independent. In addition, we have shown for the first time that caspase 2, an initiator caspase, localizes to the centrosomes in mitotic primary mouse embryonic fibroblasts, irrespective of MMR status and UVB treatment.
许多研究表明，DNA 错配修复（MMR）的作用不仅限于修复几种类型的 DNA 损伤，包括紫外线（UV）辐射。我们之前已经证明，MMR 依赖性的 UVB 诱导凋亡是抑制 UVB 诱导肿瘤形成的重要组成部分。在这里，我们证明 Msh6 依赖性的 UVB 诱导凋亡途径是通过线粒体和 p53 非依赖性途径激活的。此外，我们首次表明，起始半胱氨酸蛋白酶 caspase 2 无论 MMR 状态和 UVB 处理如何，都定位于有丝分裂原代小鼠胚胎成纤维细胞的中心体。
