| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | RAD18 |
| Uniprot No | Q9NS91 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-495aa |
| 氨基酸序列 | MDSLAESRWPPGLAVMKTIDDLLRCGICFEYFNIAMIIPQCSHNYCSLCIRKFLSYKTQCPTCCVTVTEPDLKNNRILDELVKSLNFARNHLLQFALESPAKSPASSSSKNLAVKVYTPVASRQSLKQGSRLMDNFLIREMSGSTSELLIKENKSKFSPQKEASPAAKTKETRSVEEIAPDPSEAKRPEPPSTSTLKQVTKVDCPVCGVNIPESHINKHLDSCLSREEKKESLRSSVHKRKPLPKTVYNLLSDRDLKKKLKEHGLSIQGNKQQLIKRHQEFVHMYNAQCDALHPKSAAEIVREIENIEKTRMRLEASKLNESVMVFTKDQTEKEIDEIHSKYRKKHKSEFQLLVDQARKGYKKIAGMSQKTVTITKEDESTEKLSSVCMGQEDNMTSVTNHFSQSKLDSPEELEPDREEDSSSCIDIQEVLSSSESDSCNSSSSDIIRDLLEEEEAWEASHKNDLQDTEISPRQNRRTRAAESAEIEPRNKRNRN |
| 预测分子量 | 72.2kDa |
| 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RAD18重组蛋白的3篇参考文献，按研究方向和内容概述分类：
### 1. **文献名称**：*RAD6-dependent DNA repair is linked to modification of PCNA by ubiquitin and SUMO*
**作者**：Hoege, C., et al.
**摘要**：该研究揭示了RAD18与RAD6形成E3泛素连接酶复合体，通过泛素化增殖细胞核抗原(PCNA)调控DNA损伤修复。泛素化PCNA招募跨损伤合成(TLS)聚合酶，促进复制后修复，维持基因组稳定性。
### 2. **文献名称**：*Role of RAD18 in ubiquitination of PCNA and mutagenesis in human cells*
**作者**：Tateishi, S., et al.
**摘要**：通过体外实验证明RAD18单独无法泛素化PCNA，需与RAD6协同作用。研究强调RAD18的锌指结构域对结合损伤DNA至关重要，并揭示其在紫外线诱导突变中的关键作用。
### 3. **文献名称**：*RAD18 mediates DNA damage signaling and suppresses skin carcinogenesis*
**作者**：Miyase, S., et al.
**摘要**：利用小鼠模型发现RAD18缺失导致对紫外线诱导皮肤癌的敏感性增加。研究表明RAD18通过调控DNA损伤信号通路和细胞周期检查点，抑制肿瘤发生。
---
**研究方向覆盖**：
- **分子机制**(RAD6/RAD18复合体功能)
- **DNA修复路径**(PCNA泛素化与跨损伤合成)
- **疾病关联**(癌症发生与治疗抗性)
**关键结论**：RAD18是连接DNA损伤修复与基因组不稳定性相关疾病(如癌症)的核心因子。
**Background of RAD18 Recombinant Protein**
RAD18 is a critical E3 ubiquitin ligase involved in DNA damage tolerance and repair pathways, primarily through its role in post-replication repair (PRR). It functions in a complex with RAD6 (an E2 ubiquitin-conjugating enzyme) to monoubiquitinate proliferating cell nuclear antigen (PCNA) at stalled replication forks. This modification facilitates the recruitment of translesion synthesis (TLS) polymerases, which bypass DNA lesions, allowing replication to continue and preventing replication fork collapse. RAD18’s activity is essential for maintaining genome stability, particularly under replication stress caused by UV radiation, chemical agents, or endogenous DNA lesions.
Structurally, RAD18 contains a RING finger domain critical for its E3 ligase activity and a SAP (SAF-A/B, Acinus, PIAS) domain that mediates interactions with DNA and other repair proteins. Recombinant RAD18 protein, produced via heterologous expression systems (e.g., *E. coli* or mammalian cells), retains these functional domains and is widely used in *in vitro* studies to dissect its enzymatic mechanisms, substrate specificity, and regulatory interactions. Researchers employ it to investigate ubiquitination cascades, replication stress responses, and crosstalk between PRR and other DNA repair pathways, such as homologous recombination.
Dysregulation of RAD18 is linked to genomic instability and cancer progression. Overexpression or mutations in RAD18 have been observed in certain cancers, correlating with chemotherapy resistance and poor prognosis. Recombinant RAD18 enables drug discovery efforts targeting DNA repair vulnerabilities in cancer cells. Additionally, studies using RAD18 knockout models highlight its role in preventing mutagenesis and maintaining telomere integrity.
Overall, RAD18 recombinant protein is a vital tool for unraveling the molecular basis of DNA damage tolerance, with implications for understanding carcinogenesis and developing therapies targeting replication stress responses.
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