| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | BEND3 |
| Uniprot No | Q5T5X7 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 328-461aa |
| 氨基酸序列 | CLPQLNDFFSRFWAQREMEDSQPSGQVASFFEAEQVDPGHFLDNKDQEEALSLDRSSTIASDHVVDTQDLTEFLDEASSPGEFAVFLLHRLFPELFDHRKLGEQYSCYGDGGKQELDPQRLQIIRNYTEIYFPD |
| 预测分子量 | 17.5kDa |
| 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BEND3重组蛋白的3篇代表性文献的简要信息(内容基于公开研究整理，非真实文献)：
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1. **文献名称**: *BEND3 is a novel transcriptional repressor critical for Polycomb-mediated gene silencing*
**作者**: Sakaguchi et al.
**摘要**: 本研究揭示了BEND3重组蛋白作为转录抑制因子，通过与Polycomb抑制复合体(PRC2)相互作用，调控染色质修饰和基因沉默。实验表明，重组BEND3在体外能特异性结合富含CpG的启动子区域，抑制靶基因表达，并在维持胚胎干细胞多能性中发挥关键作用。
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2. **文献名称**: *Recombinant BEND3 promotes oncogenesis by repressing tumor suppressor networks*
**作者**: Wang et al.
**摘要**: 通过表达纯化的BEND3重组蛋白，研究者发现其通过招募组蛋白去乙酰化酶(HDACs)抑制p53和PTEN等抑癌基因的转录活性。体内实验表明，BEND3过表达显著促进癌细胞增殖和转移，提示其作为潜在癌症治疗靶点。
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3. **文献名称**: *Structural and functional analysis of BEND3 in DNA damage response*
**作者**: Lee et al.
**摘要**: 该研究解析了BEND3重组蛋白的晶体结构，发现其N端BEN结构域对DNA结合至关重要。功能实验表明，BEND3通过与ATM激酶相互作用，调控DNA损伤修复通路。重组蛋白的突变体实验进一步验证了其磷酸化修饰在细胞周期检查点中的调控机制。
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**备注**：以上文献为示例性内容，实际研究中请通过PubMed或Web of Science检索真实发表的论文。若需具体文献，可提供数据库访问权限以便进一步查询。
BEND3 (BEN Domain-Containing Protein 3) is a transcriptional repressor belonging to the BEN domain protein family, which plays critical roles in chromatin organization and gene regulation. Identified in the early 2010s, BEND3 is characterized by its unique BEN domain—a structural motif involved in DNA binding and protein-protein interactions. Studies suggest it functions as a epigenetic regulator by recruiting chromatin-modifying complexes, such as polycomb repressive complexes (PRCs), to specific genomic regions, thereby silencing target genes through histone modification (e.g., H3K27me3) and chromatin compaction. It is particularly implicated in cell cycle regulation, DNA damage response, and maintaining stem cell pluripotency.
BEND3 binds to GC-rich DNA sequences, often near promoter regions, and interacts with proteins like HP1 (Heterochromatin Protein 1) to stabilize heterochromatin structures. Its activity is tightly regulated by post-translational modifications, including phosphorylation and ubiquitination. Dysregulation of BEND3 has been linked to cancers, where its overexpression may suppress tumor suppressor genes or disrupt genomic stability. Conversely, its role in embryonic development highlights its dual functionality as both a guardian of chromatin integrity and a potential oncogenic driver depending on cellular context.
Recombinant BEND3 proteins are commonly produced in *E. coli* or mammalian expression systems for *in vitro* studies, enabling biochemical assays (e.g., ChIP-seq, EMSA) to map DNA-binding sites or analyze interaction networks. Such tools are vital for dissecting its mechanisms in epigenetic silencing and exploring therapeutic strategies targeting BEND3-associated pathways in diseases like cancer or developmental disorders.
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