Brca1卷曲结构域的突变阻碍了Rad51在DNA上的装载和小鼠的发育。

Molecular & cellular oncology Pub Date : 2020-07-20 eCollection Date: 2020-01-01 DOI:10.1080/23723556.2020.1786345
J J Krais, N Johnson
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引用次数: 0

摘要

我们最近开发了Brca1卷曲线圈突变小鼠模型(Brca1CC)。Brca1CC/CC导致胚胎死亡,一小部分小鼠出生后会出现类似范可尼贫血的缺陷。Brca1CC/CC细胞缺乏Rad51病灶,对PARP抑制剂敏感。引人注目的是,与Brca1Δ11杂交产生的Brca1 CC/Δ11小鼠发育正常。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

<i>Brca1</i> mutations in the coiled-coil domain impede Rad51 loading on DNA and mouse development.

<i>Brca1</i> mutations in the coiled-coil domain impede Rad51 loading on DNA and mouse development.

Brca1 mutations in the coiled-coil domain impede Rad51 loading on DNA and mouse development.

We recently developed a Brca1 coiled-coil mutant mouse model (Brca1CC ). Brca1CC/CC results in embryonic lethality, with a fraction of mice reaching birth but with defects that parallel Fanconi anemia. Brca1CC/CC cells lacked Rad51 foci and were PARP inhibitor sensitive. Strikingly, inter-crossing with Brca1Δ11 generated Brca1 CC/Δ11 mice that were developmentally normal.

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