| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | BRMS1L |
| Uniprot No | Q5PSV4 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-323aa |
| 氨基酸序列 | MPVHSRGDKKETNHHDEMEVDYAENEGSSSEDEDTESSSVSEDGDSSEMDDEDCERRRMECLDEMSNLEKQFTDLKDQLYKERLSQVDAKLQEVIAGKAPEYLEPLATLQENMQIRTKVAGIYRELCLESVKNKYECEIQASRQHCESEKLLLYDTVQSELEEKIRRLEEDRHSIDITSELWNDELQSRKKRKDPFSPDKKKPVVVSGPYIVYMLQDLDILEDWTTIRKAMATLGPHRVKTEPPVKLEKHLHSARSEEGRLYYDGEWYIRGQTICIDKKDECPTSAVITTINHDEVWFKRPDGSKSKLYISQLQKGKYSIKHS |
| 预测分子量 | 41.7 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BRMS1L重组蛋白的3篇参考文献的简要概括(注：文献为示例性内容，实际需根据具体研究补充)：
1. **文献名称**：BRMS1L suppresses metastasis by regulating histone modifications in lung cancer
**作者**：Zhang Y, et al.
**摘要**：研究揭示了BRMS1L作为表观遗传调控因子，通过重组蛋白实验证实其与HDAC复合物互作，介导组蛋白去乙酰化，抑制肺癌细胞迁移和侵袭。
2. **文献名称**：Structural insights into BRMS1L in the mSin3A chromatin remodeling complex
**作者**：Li H, et al.
**摘要**：通过重组表达BRMS1L蛋白并进行晶体结构解析，发现其C端结构域是结合mSin3A的关键区域，为肿瘤抑制机制提供结构基础。
3. **文献名称**：BRMS1L regulates apoptosis via modulating BCL2 transcription in breast cancer
**作者**：Wang X, et al.
**摘要**：利用重组BRMS1L蛋白进行体外DNA结合实验，证明其直接抑制BCL2启动子活性，从而促进乳腺癌细胞凋亡，提示其治疗潜力。
(注：以上内容为模拟示例，实际文献需在PubMed、Web of Science等平台以关键词“BRMS1L recombinant”或“BRMS1L protein”检索核实。)
BRMS1L (BRMS1-like protein) is a member of the BRMS1 family of tumor suppressor genes, sharing structural and functional homology with BRMS1 (Breast Cancer Metastasis Suppressor 1). Both proteins are implicated in regulating chromatin remodeling, transcriptional repression, and metastasis suppression, though BRMS1L exhibits distinct molecular interactions. It is characterized by conserved coiled-coil domains and nuclear localization signals, enabling its role in epigenetic regulation.
BRMS1L interacts with components of the mSin3A-HDAC chromatin-modifying complex, facilitating histone deacetylation and gene silencing. This activity links BRMS1L to the suppression of oncogenic pathways, including those promoting cell proliferation, invasion, and epithelial-mesenchymal transition (EMT). Studies suggest its involvement in DNA damage response and apoptosis regulation, potentially through SUMOylation or ubiquitination pathways.
Recombinant BRMS1L protein is engineered for in vitro studies to dissect its biochemical properties and therapeutic potential. Produced via bacterial or mammalian expression systems, it retains functional domains necessary for binding partner recruitment (e.g., HDACs, transcription factors) and chromatin association. Researchers utilize this tool to explore its metastasis-inhibiting mechanisms, including repression of NF-κB and PI3K/Akt signaling.
Emerging evidence highlights BRMS1L's downregulation in multiple cancers (e.g., breast, lung), correlating with poor prognosis. Its recombinant form aids in functional rescue experiments, drug screening for epigenetic therapies, and structural analysis to design mimetic peptides. Ongoing research aims to clarify its tissue-specific roles and utility as a biomarker or therapeutic target in precision oncology.
×
