FOXD3通过促进mre11介导的DNA末端切除，促进同源重组修复和基因组稳定性。

IF 3.3 2区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Acta biochimica et biophysica Sinica Pub Date : 2025-06-13 DOI:10.3724/abbs.2025063

Shibin Xu, Jingyu Zhang, Congwen Gao, Ziyi Xiong, Yamin Gong, Bao Chai, Hongxiang Chen, Xingzhi Xu

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引用次数: 0

摘要

同源重组是DNA双链断裂（DSBs）高保真修复的关键，是维持基因组稳定性的重要手段。在这项研究中，我们发现FOXD3与聚（adp -核糖）聚合酶1 （PARP1）相互作用，并以PARP1依赖的方式被招募到dsb中。FOXD3直接与DSB修复蛋白MRE11结合，并促进其招募到DSB位点，确保适当的末端切除。FOXD3表达的抑制会损害hr介导的DSB修复和染色体稳定性，并使癌细胞对电离辐射敏感。总之，我们的研究结果表明FOXD3促进hr介导的DSB修复和基因组稳定性。

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FOXD3 promotes homologous recombination repair and genomic stability by facilitating MRE11-mediated DNA end resection.

Homologous recombination (HR) is crucial for the high-fidelity repair of DNA double-strand breaks (DSBs), ensuring the maintenance of genome stability. In this study, we show that FOXD3 interacts with poly (ADP-ribose) polymerase 1 (PARP1) and is recruited to DSBs in a PARP1-dependent manner. FOXD3 directly binds to the DSB repair protein MRE11 and promotes its recruitment to DSB sites, ensuring proper end resection. Inhibition of FOXD3 expression compromises HR-mediated DSB repair and chromosome stability and sensitizes cancer cells to ionizing radiation. Collectively, our findings demonstrate that FOXD3 promotes HR-mediated DSB repair and genome stability.

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来源期刊

Acta biochimica et biophysica Sinica 生物-生化与分子生物学

CiteScore

5.00

自引率

5.40%

发文量

170

审稿时长

3 months

期刊介绍： Acta Biochimica et Biophysica Sinica (ABBS) is an internationally peer-reviewed journal sponsored by the Shanghai Institute of Biochemistry and Cell Biology (CAS). ABBS aims to publish original research articles and review articles in diverse fields of biochemical research including Protein Science, Nucleic Acids, Molecular Biology, Cell Biology, Biophysics, Immunology, and Signal Transduction, etc.