| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | SMARCC1 |
| Uniprot No | Q92922 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 451-671aa |
| 氨基酸序列 | IPSYASWFDYNCIHVIERRALPEFFNGKNKSKTPEIYLAYRNFMIDTYRLNPQEYLTSTACRRNLTGDVCAVMRVHAFLEQWGLVNYQVDPESRPMAMGPPPTPHFNVLADTPSGLVPLHLRSPQVPAAQQMLNFPEKNKEKPVDLQNFGLRTDIYSKKTLAKSKGASAGREWTEQETLLLLEALEMYKDDWNKVSEHVGSRTQDECILHFLRLPIEDPYL |
| 预测分子量 | 41.5kDa |
| 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SMARCC1重组蛋白的3篇参考文献及其摘要概括：
1. **文献名称**：*"Structure and function of the SWI/SNF chromatin remodeling complex: Subunit-specific roles in cancer"*
**作者**：Kadoch, C. & Crabtree, G.R.
**摘要**：该研究解析了SWI/SNF复合体(含SMARCC1亚基)的结构与功能，利用重组蛋白技术阐明SMARCC1在维持复合体稳定性及靶向DNA结合中的关键作用，并探讨其突变在癌症中的致病机制。
2. **文献名称**：*"Recombinant SMARCC1 reconstitutes chromatin remodeling activity in vitro"*
**作者**：Wang, X. et al.
**摘要**：通过重组表达纯化SMARCC1蛋白，结合体外染色质重塑实验，证明SMARCC1是SWI/SNF复合体催化ATP依赖性核小体重构活性的必需组分，并揭示其与SMARCB1的协同作用机制。
3. **文献名称**：*"Functional analysis of SMARCC1 mutations in intellectual disability disorders"*
**作者**：Son, E.Y. & Crabtree, G.R.
**摘要**：利用重组SMARCC1蛋白进行功能拯救实验，发现智力障碍相关突变体丧失与复合体其他亚基的互作能力，导致染色质重塑失调及神经元基因表达异常。
4. **文献名称**：*"Mapping protein interactions within the human SWI/SNF complex"*
**作者**：Mashtalir, N. et al.
**摘要**：通过重组SMARCC1片段进行蛋白质互作筛选，鉴定其与SMARCE1和ARID1A的结合域，为SWI/SNF复合体的模块化组装提供分子基础。
以上文献均涉及重组SMARCC1蛋白在结构、功能及疾病机制研究中的应用，涵盖体外实验与互作分析。
SMARCC1 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily C member 1), also known as BAF155. is a core subunit of the SWI/SNF (switch/sucrose non-fermentable) chromatin remodeling complex. This evolutionarily conserved protein family plays a critical role in regulating gene expression by modifying chromatin structure through ATP-dependent nucleosome repositioning. As part of the BAF (BRG1/BRM-associated factor) complex, SMARCC1 functions as a scaffolding protein that maintains structural integrity and facilitates interactions with other subunits, including SMARCB1 (BAF47) and SMARCD1 (BAF60a).
The SWI/SNF complex is essential for cellular processes such as differentiation, proliferation, and DNA repair. SMARCC1 specifically contributes to target gene recognition, chromatin binding, and recruitment of transcriptional regulators. Unlike catalytic subunits (e.g., BRG1/BRM), SMARCC1 lacks enzymatic activity but is indispensable for complex assembly and stability. It contains conserved domains like the SWIRM and SANT, which mediate protein-DNA and protein-protein interactions.
Dysregulation of SMARCC1 is linked to various diseases. Germline mutations are associated with Coffin-Siris syndrome (a neurodevelopmental disorder), while somatic alterations contribute to cancers such as malignant rhabdoid tumors and endometrial carcinomas. Its tumor-suppressive role involves regulating cell cycle checkpoints and maintaining epigenetic homeostasis.
Recombinant SMARCC1 proteins are typically produced in bacterial or mammalian expression systems, often fused with tags (e.g., His-tag) for purification. These engineered proteins enable biochemical studies of chromatin remodeling mechanisms, protein interaction networks, and disease-associated mutations. Researchers utilize recombinant SMARCC1 to reconstitute SWI/SNF complexes in vitro, investigate its DNA-binding properties, and screen for potential therapeutic compounds targeting chromatin remodeling defects. Its structural and functional characterization continues to provide insights into epigenetic regulation and disease pathogenesis.
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