Interactions between canine RAD51 and full length or truncated BRCA2 BRC repeats

被引:10
作者
Ochiai, K. [2 ]
Yoshikawa, Y. [3 ]
Oonuma, T. [4 ]
Tomioka, Y. [1 ]
Hashizume, K. [5 ,6 ]
Morimatsu, M. [1 ]
机构
[1] Hokkaido Univ, Inst Med Genet, Sapporo, Hokkaido 0600815, Japan
[2] Univ Tokushima, Inst Hlth Biosci, Div Anim Res Resources, Grad Sch, Tokushima 7708503, Japan
[3] Kitasato Univ, Sch Vet Med, Vet Biochem Lab, Aomori 0348628, Japan
[4] Ehime Univ, Dept Biol Resources, Integrated Ctr Sci, Toon City, Ehime 7910295, Japan
[5] Iwate Univ, Dept Vet Physiol, Fac Agr, Morioka, Iwate 0208550, Japan
[6] Gifu Univ, United Grad Sch Vet Sci, Gifu 5011193, Japan
关键词
Canine; BRCA2; RAD51; RECOMBINATION; REPAIR; DNA;
D O I
10.1016/j.tvjl.2010.11.001
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
In humans, mutations in the gene for the breast cancer susceptibility protein BRCA2 affect its interactions with the recombinase RAD51 and are associated with an increased risk of cancer. This interaction occurs through a series of eight BRC repeat sequences in BRCA2. A mammalian two-hybrid assay using individual BRC repeats demonstrated that BRC6 did not bind to RAD51, whereas there was strong (BRC1, 2 and 4), intermediate (BRC8), or weak (BRC3, 5 and 7) binding of other BRC repeats to RAD51. In serial deletion mutation experiments, binding strengths were increased when the C-terminal BRC repeat was removed from BRC1-8, BRC1-5 and BRC1-3. These results may provide an insight into the effects of missense or truncation mutations in BRCA2 in canine tumours. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:293 / 295
页数:3
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