| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | MSH2 |
| Uniprot No | P43246 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-934aa |
| 氨基酸序列 | MAVQPKETLQLESAAEVGFVRFFQGMPEKPTTTVRLFDRGDFYTAHGEDA LLAAREVFKTQGVIKYMGPAGAKNLQSVVLSKMNFESFVKDLLLVRQYRV EVYKNRAGNKASKENDWYLAYKASPGNLSQFEDILFGNNDMSASIGVVGV KMSAVDGQRQVGVGYVDSIQRKLGLCEFPDNDQFSNLEALLIQIGPKECV LPGGETAGDMGKLRQIIQRGGILITERKKADFSTKDIYQDLNRLLKGKKG EQMNSAVLPEMENQVAVSSLSAVIKFLELLSDDSNFGQFELTTFDFSQYM KLDIAAVRALNLFQGSVEDTTGSQSLAALLNKCKTPQGQRLVNQWIKQPL MDKNRIEERLNLVEAFVEDAELRQTLQEDLLRRFPDLNRLAKKFQRQAAN LQDCYRLYQGINQLPNVIQALEKHEGKHQKLLLAVFVTPLTDLRSDFSKF QEMIETTLDMDQVENHEFLVKPSFDPNLSELREIMNDLEKKMQSTLISAA RDLGLDPGKQIKLDSSAQFGYYFRVTCKEEKVLRNNKNFSTVDIQKNGVK FTNSKLTSLNEEYTKNKTEYEEAQDAIVKEIVNISSGYVEPMQTLNDVLA QLDAVVSFAHVSNGAPVPYVRPAILEKGQGRIILKASRHACVEVQDEIAF IPNDVYFEKDKQMFHIITGPNMGGKSTYIRQTGVIVLMAQIGCFVPCESA EVSIVDCILARVGAGDSQLKGVSTFMAEMLETASILRSATKDSLIIIDEL GRGTSTYDGFGLAWAISEYIATKIGAFCMFATHFHELTALANQIPTVNNL HVTALTTEETLTMLYQVKKGVCDQSFGIHVAELANFPKHVIECAKQKALE LEEFQYIGESQGYDIMEPAAKKCYLEREQGEKIIQEFLSKVKQMPFTEMS EENITIKLKQLKAEVIAKNNSFVNEIISRIKVTT |
| 预测分子量 | 129 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MSH2重组蛋白的3篇参考文献，按文献发表时间顺序排列：
---
1. **文献名称**：*Reconstitution of human DNA mismatch repair in vitro using recombinant proteins*
**作者**：Gu L. et al.
**摘要**：该研究利用重组表达的MSH2、MSH6、MLH1和PMS2蛋白，在体外重建了人DNA错配修复(MMR)系统，验证了MSH2-MSH6异源二聚体对错配碱基的识别能力，并阐明了其与下游蛋白的协同作用机制。
2. **文献名称**：*Structural analysis of MSH2-MSH6 reveals a conserved ATPase domain in mismatch repair proteins*
**作者**：Warren J.J. et al.
**摘要**：通过X射线晶体学解析了MSH2-MSH6重组蛋白的ATP酶结构域的三维结构，揭示了其在DNA结合和错配修复过程中依赖ATP水解的构象变化，为理解突变导致遗传性癌症的机制提供了结构基础。
3. **文献名称**：*Functional characterization of MSH2 mutations in Lynch syndrome using recombinant protein assays*
**作者**：Raevaara T.E. et al.
**摘要**：研究通过表达纯化携带不同致病突变的MSH2重组蛋白，分析了其对DNA错配结合活性和修复功能的影响，建立了突变表型与临床林奇综合征(Lynch syndrome)的关联性。
---
**注**：以上文献为示例，实际引用时请核对具体期刊名称、作者及发表年份。如需近期研究，建议在PubMed或Web of Science中以“MSH2 recombinant protein”为关键词筛选最新文献。
**Background of MSH2 Recombinant Protein**
MSH2 (MutS homolog 2) is a critical component of the DNA mismatch repair (MMR) system, essential for maintaining genomic stability by correcting base-pair mismatches and insertion-deletion loops during DNA replication. It functions as a heterodimer, primarily pairing with MSH6 to form the MutSα complex, which recognizes mismatched nucleotides and initiates repair. Defects in MSH2 are strongly linked to Lynch syndrome (hereditary non-polyposis colorectal cancer), increasing susceptibility to colorectal, endometrial, and other cancers due to microsatellite instability (MSI) caused by impaired MMR.
Recombinant MSH2 protein is produced via genetic engineering, often using expression systems like *E. coli* or mammalian cells, to generate purified, functional protein for research and diagnostic applications. Its production enables detailed study of MMR mechanisms, including interactions with partner proteins (e.g., MSH6. MLH1) and ATP-dependent repair processes. Researchers use recombinant MSH2 to investigate how mutations disrupt MMR, assess therapeutic targets, or develop assays to screen for MSI in tumors.
In biotechnology, recombinant MSH2 aids in designing diagnostics for Lynch syndrome and evaluating cancer risk. It also supports drug discovery, particularly in identifying compounds that modulate MMR activity. By providing a controlled, high-purity source of the protein, recombinant MSH2 advances both basic understanding of DNA repair and clinical strategies to address MMR-deficient cancers.
×
