| 纯度 | >85%SDS-PAGE. |
| 种属 | Human |
| 靶点 | BCL6 |
| Uniprot No | P41182 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-418aa |
| 氨基酸序列 | MASPADSCIQFTRHASDVLLNLNRLRSRDILTDVVIVVSREQFRAHKTVLMACSGLFYSIFTDQLKCNLSVINLDPEINPEGFCILLDFMYTSRLNLREGNIMAVMATAMYLQMEHVVDTCRKFIKASEAEMVSAIKPPREEFLNSRMLMPQDIMAYRGREVVENNLPLRSAPGCESRAFAPSLYSGLSTPPASYSMYSHLPVSSLLFSDEEFRDVRMPVANPFPKERALPCDSARPVPGEYSRPTLEVSPNVCHSNIYSPKETIPEEARSDMHYSVAEGLKPAAPSARNAPYFPCDKASKEEERPSSEDEIALHFEPPNAPLNRKGLVSPQSPQKSDCQPNSPTESCSSKNACILQASGSPPAKSPTDPKACNWKKYKFIVLNSLNQNAKPEGPEQAELGRLSPRAYTAPPACQPPM |
| 预测分子量 | 59.3 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BCL6重组蛋白的3篇参考文献及其摘要概述：
1. **文献名称**：A small-molecule inhibitor of BCL6 kills lymphoma cells in vitro and in vivo
**作者**：Cerchietti, L. et al.
**摘要**：该研究通过重组BCL6蛋白筛选小分子抑制剂，发现特定化合物可破坏BCL6与其辅抑制因子的相互作用，诱导淋巴瘤细胞凋亡，并在小鼠模型中抑制肿瘤生长。
2. **文献名称**：Structural basis of BCL6-mediated transcriptional repression and its disruption in diffuse large B-cell lymphoma
**作者**：Hatzi, K. et al.
**摘要**：利用重组BCL6蛋白的BTB结构域进行X射线晶体学分析，揭示了BCL6通过同源二聚化招募辅抑制蛋白的分子机制，并发现淋巴瘤相关突变破坏此结构导致异常转录抑制。
3. **文献名称**：BCL6 BTB domain structure and interactions with corepressors: a novel binding mode
**作者**：Bereshchenko, O. et al.
**摘要**：通过重组BCL6的BTB结构域与SMRT肽复合物的结构解析，发现其采用独特的侧向沟槽结合辅抑制因子，揭示了BCL6表观遗传调控的自抑制机制，为靶向药物设计提供依据。
BCL6 (B-cell lymphoma 6) is a transcriptional repressor critical for immune regulation and lymphomagenesis. It is predominantly expressed in germinal center B-cells, where it controls differentiation, class-switch recombination, and somatic hypermutation during antibody responses. Structurally, BCL6 contains an N-terminal BTB/POZ domain that mediates homodimerization and interactions with corepressors (e.g., SMRT, NCOR), a central RD2 repression domain, and C-terminal zinc finger motifs for DNA binding. Its transcriptional repression is achieved by recruiting histone deacetylases (HDACs) and other chromatin-modifying enzymes to suppress target genes involved in cell cycle arrest, DNA damage response, and inflammatory signaling.
Dysregulation of BCL6 is a hallmark of diffuse large B-cell lymphoma (DLBCL), where chromosomal translocations or mutations stabilize its expression, leading to unchecked proliferation and blocked differentiation. As an oncogene, BCL6 also shows aberrant activity in other cancers, including T-cell lymphomas and solid tumors. Research on recombinant BCL6 protein focuses on elucidating its molecular interactions, structural dynamics, and regulatory mechanisms. Recombinant versions, often produced in *E. coli* or mammalian systems, retain functional domains and are essential for *in vitro* studies, such as binding assays, inhibitor screening, and structural analyses (e.g., X-ray crystallography).
Therapeutic strategies targeting BCL6 include small-molecule inhibitors disrupting corepressor binding or proteolysis-targeting chimeras (PROTACs). Recombinant BCL6 proteins serve as tools for validating these inhibitors and mapping interaction interfaces. Additionally, they aid in studying post-translational modifications (e.g., acetylation, ubiquitination) that modulate BCL6 stability and activity. Understanding BCL6's dual role in normal immunity and malignancy underscores its importance as a biomarker and therapeutic target, driving ongoing research into its biology and clinical applications.
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