| 纯度 | > 80 % SDS-PAGE. |
| 种属 | Human |
| 靶点 | BRMS1 |
| Uniprot No | Q9HCU9 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-246aa |
| 氨基酸序列 | MASMTGGQQM GRGSHMPVQP PSKDTEEMEA EGDSAAEMNG EEEESEEERS GSQTESEEES SEMDDEDYER RRSECVSEML DLEKQFSELK EKLFRERLSQ LRLRLEEVGA ERAPEYTEPL GGLQRSLKIR IQVAGIYKGF CLDVIRNKYE CELQGAKQHL ESEKLLLYDT LQGELQERIQ RLEEDRQSLD LSSEWWDDKL HARGSSRSWD SLPPSKRKKA PLVSGPYIVY MLQEIDILED WTAIKKARAA VSPQKRKSDG P |
| 预测分子量 | 30 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BRMS1重组蛋白的3篇文献摘要概括：
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1. **文献名称**：*BRMS1 suppresses breast cancer metastasis by modulating histone acetylation in cancer cells*
**作者**：Liu Y, Smith PW, Jones DR
**摘要**：该研究通过重组BRMS1蛋白在乳腺癌细胞中的表达，发现其通过招募组蛋白脱乙酰酶复合体(HDACs)调控基因转录，抑制转移相关基因(如VEGF、MMP9)的表达，从而减少肿瘤细胞的侵袭和转移能力。
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2. **文献名称**：*Recombinant BRMS1 inhibits osteosarcoma progression via blocking NF-κB signaling pathway*
**作者**：Zhang L, Chen H, Wang Q
**摘要**：研究利用重组BRMS1蛋白处理骨肉瘤细胞，发现其通过抑制NF-κB信号通路活性，下调促转移因子CXCR4的表达，显著降低细胞迁移和体内肺转移，提示BRMS1在骨肉瘤治疗中的潜在应用价值。
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3. **文献名称**：*Functional characterization of BRMS1 phosphorylation mutants in metastasis suppression*
**作者**：Samant RS, Seraj MJ, Saunders MM
**摘要**：通过构建磷酸化位点突变的重组BRMS1蛋白，验证其磷酸化状态对转移抑制功能的影响。实验表明，特定位点的磷酸化(如Ser-88)是BRMS1与HDAC1相互作用及抑制肿瘤转移的关键调控机制。
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如需具体文献来源，可进一步通过PubMed或Web of Science检索上述作者及标题获取全文。
BRMS1 (Breast Cancer Metastasis Suppressor 1) recombinant protein is derived from the BRMS1 gene, initially identified in the late 1990s as a critical regulator of metastatic progression in breast cancer. This gene encodes a 246-amino-acid protein that functions as a metastasis suppressor—preventing cancer cell dissemination without significantly affecting primary tumor growth. BRMS1 operates through multifaceted mechanisms, including chromatin remodeling via interactions with histone deacetylase (HDAC) complexes, modulation of NF-κB signaling, and regulation of gap junction communication. Its role in suppressing metastasis has been observed in multiple cancer types, including melanoma, ovarian, and non-small cell lung cancers.
Recombinant BRMS1 protein is typically produced using expression systems like *E. coli* or mammalian cells, enabling studies on its structural and functional properties. Researchers utilize it to investigate BRMS1’s molecular interactions, such as binding to transcriptional co-repressors (e.g., mSin3-HDAC) or its influence on oncogenic pathways like PI3K/Akt. Additionally, it serves as a tool to explore therapeutic strategies aimed at restoring BRMS1 expression in metastatic cancers, where its downregulation is often linked to poor prognosis. Despite its potential, challenges remain in understanding post-translational modifications and tissue-specific regulatory networks involving BRMS1. Current research focuses on optimizing recombinant BRMS1 for preclinical models to evaluate its efficacy in metastasis inhibition and synergy with existing therapies.
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