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Moving Mountains—The BRCA1 Promotion of DNA Resection

机译:移山—BRCA1促进DNA切除

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摘要

DNA double-strand breaks (DSBs) occur in our cells in the context of chromatin. This type of lesion is toxic, entirely preventing genome continuity and causing cell death or terminal arrest. Several repair mechanisms can act on DNA surrounding a DSB, only some of which carry a low risk of mutation, so that which repair process is utilized is critical to the stability of genetic material of cells. A key component of repair outcome is the degree of DNA resection directed to either side of the break site. This in turn determines the subsequent forms of repair in which DNA homology plays a part. Here we will focus on chromatin and chromatin-bound complexes which constitute the “mountains” that block resection, with a particular focus on how the breast and ovarian cancer predisposition protein-1 (BRCA1) contributes to repair outcomes through overcoming these blocks.
机译:DNA双链断裂(DSB)在染色质的背景下在我们的细胞中发生。这种类型的病变是有毒的,完全阻止了基因组的连续性并导致细胞死亡或终末停止。几种修复机制可以作用于DSB周围的DNA,只有其中一些具有较低的突变风险,因此,利用哪种修复过程对细胞遗传物质的稳定性至关重要。修复结果的关键组成部分是指向断裂部位两侧的DNA切除程度。反过来,这决定了DNA同源性发挥作用的后续修复形式。在这里,我们将重点研究染色质和与染色质结合的复合物,它们构成阻断切除的“山峰”,尤其着重于乳腺癌和卵巢癌易感蛋白1(BRCA1)如何通过克服这些阻断来修复结果。

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