MRI is a DNA Damage Response Adaptor during Classical Non-Homologous End Joining. Hung et al.

These are the original data files for the Molecular Cell manuscript titled "MRI is a DNA Damage Response Adaptor during Classical Non-Homologous End Joining" by Hung et al. The paper characterizes the role of a small disordered peptide MRI (modulator of retrovirus infection, also known as CYREN) in promoting non-homologous end joining (NHEJ). Specifically, MRI associates with diverse DNA damage response factors at its termini and increases their avidity for chromatin at DNA double-strand breaks (DSBs). Moreover, MRI functions redundantly with XLF in DSB repair, and the loss of both proteins severely impairs V(D)J recombination in lymphocytes and leads to embryonic lethality in mice. We thus purpose that MRI acts as an adaptor that helps to enhance the efficiency of NHEJ.

本数据集包含Hung等人发表于学术期刊《分子细胞》（*Molecular Cell*）、题为《MRI在经典非同源末端连接过程中作为DNA损伤应答接头蛋白》的研究论文的原始数据文件。该论文阐明了小型无序肽段MRI（modulator of retrovirus infection, 亦称CYREN）在促进非同源末端连接（non-homologous end joining, NHEJ）中的功能。具体而言，MRI可通过其末端区域与多种DNA损伤应答因子结合，并增强这些因子在DNA双链断裂（DNA double-strand breaks, DSBs）位点对染色质的结合亲和力。此外，MRI在DNA双链断裂修复过程中与XLF发挥冗余功能；二者同时缺失会显著损伤淋巴细胞中的V(D)J重组，并引发小鼠胚胎致死。据此我们提出，MRI可作为接头蛋白，提升非同源末端连接的修复效率。