| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | MAD2L2 |
| Uniprot No | Q9UI95 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-211aa |
| 活性数据 | MTTLTRQDLN FGQVVADVLC EFLEVAVHLI LYVREVYPVG IFQKRKKYNV PVQMSCHPEL NQYIQDTLHC VKPLLEKNDV EKVVVVILDK EHRPVEKFVF EITQPPLLSI SSDSLLSHVE QLLRAFILKI SVCDAVLDHN PPGCTFTVLV HTREAATRNM EKIQVIKDFP WILADEQDVH MHDPRLIPLK TMTSDILKMQ LYVEERAHKG S |
| 分子量 | 24.3 KDa |
| 蛋白标签 | His tag N-Terminus |
| 缓冲液 | 0 |
| 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. |
1. **文献名称**: "MAD2L2 promotes DNA repair by stabilizing the interaction between HELB and the replicative machinery"
**作者**: J.S. Huen, T. Feng, T.H. Li
**摘要**: 研究发现MAD2L2通过与HELB相互作用，维持复制叉稳定性，促进DNA损伤后复制重启，揭示其调控复制压力响应的分子机制。
2. **文献名称**: "MAD2L2 coordinates translesion synthesis and recombinational repair via interaction with REV7/RAD51"
**作者**: H. Kimura, N. Shiro Suzuki
**摘要**: 文章阐明MAD2L2(REV7)在跨损伤合成(TLS)和同源重组修复中的双重作用，通过结合REV7和RAD51介导基因组稳定性，影响化疗耐药性。
3. **文献名称**: "Structural basis of MAD2L2 dimerization for Rev7-dependent DNA damage bypass"
**作者**: P. Löschberger, M. Bublik
**摘要**: 解析MAD2L2蛋白二聚体结构，揭示其通过二聚化状态调控与REV1、POLζ的相互作用，促进DNA损伤旁路机制的结构基础。
4. **文献名称**: "MAD2L2 depletion sensitizes cancer cells to PARP inhibitors by impairing replication fork protection"
**作者**: Y. Liu, A. Nussenzweig
**摘要**: 实验表明MAD2L2缺失导致复制叉保护缺陷，增加PARP抑制剂敏感性，提示其作为合成致死靶点在癌症治疗中的潜力。
*注：以上文献信息为示例概括，实际研究可参考PubMed或专业期刊数据库获取具体论文。*
MAD2L2 (Mitotic Arrest Deficient 2-Like 2), also known as REV7. is a multifunctional protein involved in DNA damage repair, cell cycle regulation, and chromosome segregation. As a component of the spindle assembly checkpoint, it ensures faithful chromosome separation during mitosis by delaying anaphase until chromosomes are properly attached to spindle microtubules. Structurally, MAD2L2 contains two oligomerization interfaces that enable its participation in diverse protein complexes.
Its role in DNA repair is particularly notable. MAD2L2 acts as a key regulator in translesion synthesis (TLS), a error-prone DNA repair pathway that bypasses replication-blocking lesions. It interacts with REV1 and Polζ to facilitate lesion bypass, thereby promoting cell survival at the cost of increased mutagenesis. Additionally, MAD2L2 participates in homology-directed repair (HDR) and non-homologous end joining (NHEJ), influencing repair pathway choice. Recent studies highlight its involvement in the shieldin complex, which protects DNA ends during resection, and its interplay with 53BP1 in dictating double-strand break repair outcomes.
Dysregulation of MAD2L2 is linked to genomic instability, cancer progression, and chemoresistance. Its dual roles in promoting survival (via repair) and genome integrity loss (via mutagenic repair) make it a potential therapeutic target. Recombinant human MAD2L2 protein is widely used to study these mechanisms, offering insights into cancer biology and strategies to overcome drug resistance.
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