| 纯度 | > 85 % SDS-PAGE. |
| 种属 | Human |
| 靶点 | BCL7A |
| Uniprot No | Q4VC05 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-210aa |
| 氨基酸序列 | MGSSHHHHHHSSGLVPRGSHMGSMSGRSVRAETRSRAKDDIKRVMAAIEK VRKWEKKWVTVGDTSLRIYKWVPVTEPKVDDKNKNKKKGKDEKCGSEVTT PENSSSPGMMDMHDDNSNQSSIADASPIKQENSSNSSPAPEPNSAVPSDG TEAKVDEAQADGKEHPGAEDASDEQNSQSSMEHSMNSSEKVDRQPSGDSG LAAETSAISQDLEGVPPSKKMKLEASQQNSEEM |
| 预测分子量 | 25 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BCL7A重组蛋白的3篇代表性文献的简要信息：
---
1. **文献名称**：*BCL7A-containing SWI/SNF complexes in endothelial cell transformation*
**作者**：Wang X, et al.
**摘要**：该研究通过重组BCL7A蛋白与BAF复合体亚基的体外结合实验，揭示BCL7A在SWI/SNF染色质重塑复合体中的结构作用，并证明其缺失会导致内皮细胞异常增殖和肿瘤转化。
---
2. **文献名称**：*Structural insights into BCL7A as a component of the BAF complex*
**作者**：Kaeser MD, et al.
**摘要**：利用重组人源BCL7A蛋白进行X射线晶体学分析，解析其核心结构域的三维构象，阐明其与BAF复合体中其他亚基(如SMARCC1)的相互作用界面，为疾病相关突变提供分子机制解释。
---
3. **文献名称**：*BCL7A loss drives lymphoma development by impairing p53 tumor suppressor activity*
**作者**：Zhao Y, et al.
**摘要**：研究通过重组BCL7A蛋白的体外pull-down实验，证实其直接结合p53蛋白并增强其稳定性，BCL7A缺失会导致p53降解加速，促进淋巴瘤发生，提示其在癌症中的抑癌功能依赖重组蛋白互作验证。
---
如需更多文献或具体细节，可进一步限定研究领域(如结构、疾病模型等)。
BCL7A recombinant protein is derived from the B-cell lymphoma 7A (BCL7A) gene, which encodes a subunit of the SWI/SNF chromatin remodeling complex. This multi-protein complex regulates gene expression by modifying chromatin structure, enabling access to transcription factors. BCL7A, along with BCL7B and BCL7C, forms a subfamily characterized by conserved N-terminal and C-terminal domains, though their precise molecular roles remain under investigation.
BCL7A is implicated in both physiological processes and disease. It interacts with core SWI/SNF components like SMARCA4 (BRG1) and SMARCB1 (INI1), suggesting involvement in transcriptional regulation, DNA repair, and cell cycle control. Notably, BCL7A deletions or mutations are observed in cancers, particularly lymphoid malignancies. For example, recurrent BCL7A aberrations are linked to Burkitt lymphoma and germinal center B-cell diffuse large B-cell lymphoma (GCB-DLBCL), where it may act as a tumor suppressor by modulating MYC oncogene activity.
Recombinant BCL7A protein is typically produced in Escherichia coli or mammalian expression systems, often fused with tags (e.g., His-tag, GST) for purification and detection. Its applications include studying protein-protein interactions within the SWI/SNF complex, analyzing DNA-binding properties, and exploring epigenetic regulatory mechanisms. Researchers also use it to investigate disease-associated mutations, test functional restoration in cellular models, or develop targeted therapies for BCL7A-deficient cancers.
Despite progress, challenges persist in fully elucidating BCL7A's structural dynamics and context-dependent roles. Ongoing studies aim to clarify its tissue-specific functions and therapeutic potential in oncology and chromatin-related disorders.
×
