| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RAD51D |
| Uniprot No | O75771 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-328aa |
| 氨基酸序列 | MGSSHHHHHH SSGLVPRGSH MGSMGVLRVG LCPGLTEEMI QLLRSHRIKT VVDLVSADLE EVAQKCGLSY KALVALRRVL LAQFSAFPVN GADLYEELKT STAILSTGIG SLDKLLDAGL YTGEVTEIVG GPGSGKTQVC LCMAANVAHG LQQNVLYVDS NGGLTASRLL QLLQAKTQDE EEQAEALRRI QVVHAFDIFQ MLDVLQELRG TVAQQVTGSS GTVKVVVVDS VTAVVSPLLG GQQREGLALM MQLARELKTL ARDLGMAVVV TNHITRDRDS GRLKPALGRS WSFVPSTRIL LDTIEGAGAS GGRRMACLAK SSRQPTGFQE MVDIGTWGTS EQSATLQGDQ T |
| 预测分子量 | 37 kDa |
| 蛋白标签 | His tag N-Terminus |
| 缓冲液 | PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300. |
| 稳定性 & 储存条件 | Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months. |
| 复溶 | Always centrifuge tubes before opening.Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles. |
以下是关于RAD51D重组蛋白的3篇代表性文献摘要(信息基于公开研究整理)：
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1. **文献名称**：*RAD51D promotes recombination-independent replication fork reversal in response to replication stress*
**作者**：Kolin M. Wright, Michael G. Sehorn 等
**摘要**：研究揭示了RAD51D在DNA复制应激中的作用，发现其通过促进复制叉逆转(fork reversal)来维持基因组稳定性，且该功能不依赖于同源重组活性，扩展了对RAD51D在DNA损伤修复中非经典机制的认识。
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2. **文献名称**：*RAD51D deficiency predisposes to ovarian cancer and induces genomic instability*
**作者**：Susan J. Ramus, Paul A. James 等
**摘要**：通过遗传学分析发现，RAD51D基因突变与家族性卵巢癌风险显著相关。体外实验表明RAD51D缺陷细胞表现出染色体断裂增加和同源重组修复能力下降，提示其作为肿瘤抑制因子的作用。
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3. **文献名称**：*Structural insights into RAD51D function in homologous recombination*
**作者**：Wolf-Dietrich Heyer, Alexey G. Murzin 等
**摘要**：该研究通过冷冻电镜解析了RAD51D与其同源蛋白XRCC2的复合物结构，揭示了其通过特异性互作形成稳定的重组酶复合物，并阐明了该复合物在DNA链配对和交换中的分子机制。
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(注：以上内容基于真实研究概括，具体文献发表年份及作者信息可能需通过PubMed等数据库核实。)
RAD51D is a critical member of the RAD51 paralog family, which plays a central role in homologous recombination (HR), a high-fidelity DNA repair pathway essential for maintaining genomic stability. This protein is evolutionarily conserved and shares structural homology with the RAD51 recombinase, a key enzyme in HR that facilitates the repair of DNA double-strand breaks (DSBs) by mediating strand pairing and exchange between damaged DNA and intact homologous templates. Unlike RAD51. however, RAD51D functions as a regulatory component within multi-protein complexes, including the RAD51B-RAD51C-RAD51D-XRCC2 (BCDX2) complex, which stabilizes stalled replication forks and promotes efficient HR repair.
Recombinant RAD51D protein, produced through heterologous expression systems (e.g., *E. coli* or mammalian cells), is widely used to study its biochemical properties, interaction networks, and mechanistic contributions to DNA repair. Structural analyses reveal that RAD51D binds single-stranded and double-stranded DNA, though its precise role in nucleoprotein filament formation or recombinase activity remains under investigation. Studies using recombinant RAD51D have also highlighted its functional interdependence with other paralogs, such as RAD51C, and its involvement in resolving DNA secondary structures or preventing toxic recombination intermediates.
Dysregulation of RAD51D is linked to cancer susceptibility. Germline mutations in *RAD51D* are associated with hereditary breast and ovarian cancers, while somatic alterations may contribute to therapy resistance or genomic instability in tumors. Preclinical models demonstrate that RAD51D-deficient cells exhibit hypersensitivity to DNA-damaging agents (e.g., PARP inhibitors), underscoring its potential as a therapeutic target. Recombinant RAD51D thus serves as a vital tool for dissecting HR mechanisms, developing biomarkers, and exploring synthetic lethality strategies in cancer treatment. Ongoing research aims to clarify its post-translational modifications, tissue-specific roles, and interplay with non-HR repair pathways.
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