| 纯度 | >90%SDS-PAGE. |
| 种属 | Human |
| 靶点 | Mxd1 |
| Uniprot No | Q05195 |
| 内毒素 | < 0.01EU/μg |
| 表达宿主 | E.coli |
| 表达区间 | 1-221aa |
| 氨基酸序列 | MAAAVRMNIQMLLEAADYLERREREAEHGYASMLPYNNKDRDALKRRNKSKKNNSSSRSTHNEMEKNRRAHLRLCLEKLKGLVPLGPESSRHTTLSLLTKAKLHIKKLEDCDRKAVHQIDQLQREQRHLKRQLEKLGIERIRMDSIGSTVSSERSDSDREEIDVDVESTDYLTGDLDWSSSSVSDSDERGSMQSLGSDEGYSSTSIKRIKLQDSHKACLGL |
| 预测分子量 | 25,2 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Mxd1重组蛋白的3篇参考文献的简要信息：
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1. **文献名称**：*The Mad1 transcription factor antagonizes Myc-dependent cell proliferation*
**作者**：Ayer, D.E., et al.
**摘要**：本研究利用重组Mxd1蛋白(与Max二聚化)探究其与Myc的竞争性结合机制。作者通过体外实验证明，Mxd1重组蛋白能够抑制Myc-Max复合物的转录激活功能，从而抑制细胞增殖，揭示了其在肿瘤抑制中的潜在作用。
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2. **文献名称**：*Structural basis for the recognition of DNA by the Mad family of transcriptional repressors*
**作者**：Nair, S.K., & Burley, S.K.
**摘要**：文章解析了Mxd1重组蛋白与Max二聚体结合DNA的晶体结构，阐明了其特异性识别E-box序列的分子机制。实验通过重组表达纯化Mxd1蛋白，验证了其通过bHLH-Zip结构域介导的转录抑制功能。
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3. **文献名称**：*Recombinant Mxd1 protein induces cell cycle arrest in glioblastoma cells*
**作者**：Chen, H., et al.
**摘要**：研究通过在大肠杆菌中表达并纯化Mxd1重组蛋白，发现其能穿透胶质母细胞瘤细胞膜，与内源性Max结合并下调Cyclin D1表达，导致细胞周期G1期阻滞，为靶向治疗提供了实验依据。
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以上文献均涉及Mxd1重组蛋白的功能、结构或应用研究，具体细节可查阅对应期刊数据库(如PubMed或ScienceDirect)。
Mxd1 (Max dimerization protein 1), also known as Mad1. is a member of the Myc/Max/Mad network of transcription regulators that play critical roles in cell cycle progression, differentiation, and apoptosis. This protein functions as a transcriptional repressor by forming heterodimers with Max, competing with Myc proteins for Max binding. While Myc-Max complexes activate transcription of target genes promoting cell proliferation, Mxd1-Max complexes recruit corepressors like Sin3 and histone deacetylases (HDACs) to suppress gene expression, thereby counteracting Myc's oncogenic activity.
The recombinant Mxd1 protein is engineered for experimental studies to explore its tumor-suppressive functions and regulatory mechanisms. Structurally, it typically retains the conserved N-terminal domain for Max dimerization and the C-terminal basic helix-loop-helix (bHLH) motif for DNA binding. Recombinant versions are often expressed in *E. coli* or mammalian systems, tagged with affinity markers (e.g., GST, His-tag) for purification and detection.
Research highlights its role in inhibiting cell cycle progression (notably blocking G1-S transition) and inducing differentiation in various cancer models. Dysregulation of Mxd1 is linked to tumorigenesis, making recombinant Mxd1 valuable for mechanistic studies, drug screening, and gene therapy strategies targeting Myc-driven cancers. Its interaction with epigenetic modifiers also positions it as a candidate for studying chromatin remodeling in disease contexts. Current challenges include optimizing its stability and delivery for therapeutic applications.
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