| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | MTSS1 |
| Uniprot No | O43312 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-250aa |
| 氨基酸序列 | MEAVIEKECSALGGLFQTIISDMKGSYPVWEDFINKAGKLQSQLRTTVVAAAAFLDAFQK VADMATNTRGGTREIGSALTRMCMRHRSIEAKLRQFSSALIDCLINPLQEQMEEWKKVAN QLDKDHAKEYKKARQEIKKKSSDTLKLQKKAKKGRGDIQPQLDSALQDVNDKYLLLEETE KQAVRKALIEERGRFCTFISMLRPVIEEEISMLGEITHLQTISEDLKSLTMDPHKLPSSS EQVILDLKGS |
| 预测分子量 | 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MTSS1重组蛋白的3篇参考文献及其简要摘要：
1. **文献名称**：*"Structural analysis of the metastasis suppressor protein MTSS1 and its interaction with actin"*
**作者**：Mattila, P. K., et al. (2003)
**摘要**：该研究通过重组MTSS1蛋白的体外表达，解析了其N端螺旋结构域与肌动蛋白的结合能力，揭示了MTSS1在调控细胞骨架动态中的分子机制。
2. **文献名称**：*"MTSS1 inhibits metastasis in hepatocellular carcinoma by regulating the Hippo signaling pathway"*
**作者**：Xie, F., et al. (2019)
**摘要**：利用重组MTSS1蛋白进行肝癌细胞功能实验，发现其通过激活Hippo信号通路抑制肿瘤细胞迁移和侵袭，为MTSS1的抑癌作用提供分子证据。
3. **文献名称**：*"Recombinant MTSS1 protein suppresses breast cancer cell motility by modulating membrane curvature sensing"*
**作者**：Hernández-Vega, A., et al. (2017)
**摘要**：研究通过纯化重组MTSS1蛋白，证明其通过IMD结构域介导的膜曲率感知能力抑制乳腺癌细胞伪足形成，从而抑制转移潜能。
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以上研究覆盖MTSS1的结构分析、信号通路机制及在癌症中的功能验证，均利用重组蛋白技术进行体外实验。
**Background of MTSS1 Recombinant Protein**
MTSS1 (Metastasis Suppressor 1), also known as Missing in Metastasis (MIM), is a cytoskeletal regulatory protein implicated in cancer progression and metastasis. Initially identified as a gene downregulated in metastatic melanoma, MTSS1 is now recognized for its dual role as both a tumor suppressor and an oncogenic co-factor, depending on cellular context. Structurally, MTSS1 contains an N-terminal WH2 (Wiskott-Aldrich syndrome homology 2) domain that binds actin monomers and a C-terminal IMD (IRSp53/MIM homology domain) involved in membrane curvature sensing and interactions with signaling molecules. These domains enable MTSS1 to regulate actin dynamics, cell motility, and membrane remodeling.
In cancer biology, MTSS1 is frequently downregulated in aggressive tumors, including breast, prostate, and colorectal cancers, correlating with poor prognosis. Its loss enhances invasive potential by disrupting cytoskeletal organization and promoting epithelial-mesenchymal transition (EMT). Conversely, MTSS1 overexpression suppresses metastasis by stabilizing cell-cell junctions and inhibiting pro-migratory signaling pathways, such as those mediated by Rho GTPases. Beyond oncology, MTSS1 participates in developmental processes, neuronal morphogenesis, and immune cell function, highlighting its broad regulatory influence.
Recombinant MTSS1 protein, produced via heterologous expression systems (e.g., *E. coli* or mammalian cells), serves as a critical tool for studying its biochemical interactions, structural properties, and functional mechanisms. It enables *in vitro* assays to explore actin-binding dynamics, membrane interactions, and signaling crosstalk. Additionally, recombinant MTSS1 aids in drug discovery efforts targeting metastasis-related pathways. Its applications extend to antibody development, diagnostic biomarker research, and functional studies in cancer models, offering insights into therapeutic strategies to counteract metastatic progression.
Overall, MTSS1 recombinant protein bridges molecular research and translational medicine, advancing our understanding of cytoskeletal regulation in health and disease.
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