Defining the DNA mismatch repair-dependent apoptotic pathway in primary cells: Evidence for p53-independence and involvement of centrosomal caspase 2

被引：9
|
作者：
Narine, Kelly A. D. [1 ]
Keuling, Angela M. [1 ]
Gombos, Randi [1 ]
Tron, Victor A. [2 ]
Andrew, Susan E. [1 ]
Young, Leah C. [1 ]
机构：
[1] Univ Alberta, Dept Med Genet, Edmonton, AB T6G 2H7, Canada
[2] Queens Univ, Dept Pathol & Mol Med, Kingston, ON, Canada
来源：
DNA REPAIR | 2010年 / 9卷 / 02期
基金：
加拿大健康研究院;
关键词：
DNA mismatch repair; Msh6; UVB; Apoptosis; p53; Caspase; 2; Centrosome; FEMALE EMBRYONIC LETHALITY; PROMOTER REGION; CYCLE ARREST; PROTEIN MSH6; CANCER CELLS; SKIN-CANCER; GENE HMSH2; IN-VIVO; P53; DAMAGE;
D O I：
10.1016/j.dnarep.2009.11.010
中图分类号：
Q3 [遗传学];
学科分类号：
071007 ; 090102 ;
摘要：
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. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码：161 / 168
页数：8
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