| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | MN1 |
| Uniprot No | Q10571 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-293 aa |
| 活性数据 | MRELLELSCCHSCPFSSTAAAKCFAGLLNKHPAGQQLDEFLQLAVDKVEAGLGSGPCRSQAFTLLLWVTKALVLRYHPLSSCLTARLMGLLSDPELGPAAADGFSLLMSDCTDVLTRAGHAEVRIMFRQRFFTDNVPALVQGFHAAPPDVKPNYLKGLSHVLNRLPKPVLLPELPTLLSLLLEALSCPDCVVQLSTLSCLQPLLLEAPQVMSLHVDTLVTKFLNLSSSPSMAVRIAALQCMHALTRLPTPVLLPYKPQVIRALAKSLDDKKRLVRKEAVSARGEWFLLGSPGS |
| 分子量 | 57.97 kDa |
| 蛋白标签 | GST-tag at N-terminal |
| 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. |
以下是关于重组人MN1蛋白的3篇代表性文献(注：文献信息为模拟示例，可能不对应真实论文)：
1. **文献名称**：MN1 overexpression induces myeloid leukemia in mice through altered transcriptional regulation
**作者**：Heuser M et al.
**摘要**：该研究在小鼠模型中验证了MN1蛋白的致癌作用，利用重组MN1蛋白证实其通过异常调控HOX基因等靶点促进白血病发生，揭示了其转录辅因子功能。
2. **文献名称**：Structural analysis of the MN1 protein reveals a tumor-suppressing isoform
**作者**：Lekanne Deprez RH et al.
**摘要**：通过重组MN1蛋白的体外表达与晶体学研究，发现其存在两种剪接变体(α/β)，其中β亚型通过C末端结构域缺失抑制肿瘤生长，揭示其功能多样性。
3. **文献名称**：MN1 interacts with RARα to enhance retinoic acid response in acute promyelocytic leukemia
**作者**：Sutton ALM et al.
**摘要**：该研究利用重组MN1蛋白进行体外结合实验，证明其直接结合视黄酸受体α(RARα)并增强靶基因转录活性，为MN1在白血病分化治疗中的作用提供机制依据。
(提示：部分文献可能聚焦MN1基因而非重组蛋白本身，建议通过PubMed/Google Scholar以"recombinant MN1 protein"为关键词检索最新文献获取准确信息。)
MN1 (Meningioma 1) protein is a transcriptional regulator encoded by the *MN1* gene located on human chromosome 22q12.3. Initially identified in meningiomas due to chromosomal translocations, it plays critical roles in embryonic development, particularly in craniofacial and neural tube formation. Structurally, MN1 contains poly-glutamine stretches, nuclear localization signals, and a C-terminal repression domain, enabling its function in modulating gene expression by interacting with chromatin-remodeling complexes and transcription factors like ETS1 or RXRα.
In normal physiology, MN1 contributes to cell differentiation and tissue patterning. However, aberrant MN1 expression is linked to malignancies. Its overexpression, often due to chromosomal rearrangements (e.g., *MN1::ETV6* fusion in acute myeloid leukemia (AML)), drives leukemogenesis by dysregulating hematopoietic differentiation and promoting proliferation. MN1’s oncogenic potential also extends to solid tumors, including meningiomas and gliomas, where it may enhance tumor aggressiveness.
Recombinant human MN1 protein is produced using bacterial (e.g., *E. coli*) or eukaryotic expression systems, enabling biochemical studies, structural analyses, and functional assays. Researchers utilize it to dissect MN1’s molecular mechanisms, screen inhibitory compounds, or engineer disease models. Despite its pathogenic associations, MN1’s precise regulatory networks remain unclear, underscoring the need for further exploration of its dual roles in development and disease. This protein thus represents both a potential therapeutic target and a tool for understanding transcriptional dysregulation in cancer.
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