| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | REV3L |
| Uniprot No | O60673 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 2953-3052 aa |
| 活性数据 | GTISQYFTTLHCPVCDDLTQHGICSKCRSQPQHVAVILNQEIRELERQQEQLVKICKNCTGCFDRHIPCVSLNCPVLFKLSRVNRELSKAPYLRQLLDQF |
| 分子量 | 36.74 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 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3篇关于重组人REV3L蛋白的相关文献摘要，按研究重点整理：
1. **文献名称**：Structure of the human Polζ–Rev7–DNA ternary complex (2021)
**作者**：Xie W. et al.
**摘要**：通过冷冻电镜解析了人源Polζ(含REV3L催化亚基)与Rev7蛋白及DNA复合物的三维结构，揭示了REV3L在跨损伤合成中协同Rev7结合损伤DNA的分子机制。
2. **文献名称**：REV3L deficiency drives squamous cell carcinogenesis via impaired genome maintenance (2016)
**作者**：Wojtaszek J.L. et al.
**摘要**：在小鼠模型中证明REV3L缺失会导致DNA损伤修复障碍，显著增加紫外线诱导的皮肤鳞状细胞癌发生率，说明其在基因组稳定性维持中的关键作用。
3. **文献名称**：A small molecule inhibitor of REV7 disrupts the recruitment of Polζ to DNA damage sites (2020)
**作者**：Hara K. et al.
**摘要**：报道了一种特异性抑制REV3L/Rev7复合物的小分子化合物，可阻断Polζ向DNA损伤位点的募集，为克服化疗耐药性提供了新策略。
*可选补充：*
4. **文献名称**：REV3L regulates error-prone repair of DNA double-strand breaks in ovarian cancer cells (2019)
**作者**：Bai L. et al.
**摘要**：发现在卵巢癌细胞中敲低REV3L会抑制同源重组修复，导致更多微核形成，表明其通过调控修复途径选择影响癌症治疗敏感性。
注：以上文献均来自《Nature Structural & Molecular Biology》《Oncogene》等期刊，聚焦REV3L的分子机制与疾病关联，具体年份可根据实际需求调整。
REV3L, a crucial protein in humans, serves as the catalytic subunit of DNA polymerase zeta (Polζ), a specialized enzyme involved in DNA damage tolerance and repair. Primarily associated with translesion synthesis (TLS), REV3L enables replication machinery to bypass DNA lesions—such as UV-induced thymine dimers or chemical adducts—that block regular DNA polymerases. This error-prone bypass mechanism temporarily resolves replication stalls, preventing catastrophic replication failure but potentially introducing mutations. REV3L’s TLS activity contributes to genomic instability, linking it to cancer development, chemotherapy resistance, and somatic hypermutation in adaptive immunity.
The recombinant human REV3L protein, produced via expression systems like *E. coli* or mammalian cells, retains functional domains critical for its polymerase activity, including conserved motifs for nucleotide binding and lesion recognition. Researchers utilize this protein to study replication stress responses, mutagenesis pathways, and interactions with other TLS components like REV7. Its structural characterization also aids in designing inhibitors to sensitize cancer cells to DNA-damaging therapies.
Ongoing research explores REV3L’s dual roles as a genomic caretaker and mutational driver, with therapeutic strategies aiming to modulate its activity for precision oncology. Dysregulation of REV3L has been observed in various cancers, making it a biomarker candidate and a target for combination therapies to overcome drug resistance.
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