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MDM4 (MDM4 Regulator Of P53, also known as MDMX) is a Protein Coding gene. This gene encodes a nuclear protein that contains a p53 binding domain at the N-terminus and a RING finger domain at the C-terminus and shows structural similarity to p53-binding protein MDM2. MDM4 is a promising target for cancer therapy, as it is undetectable in most normal adult tissues but often upregulated in cancer cells to dampen p53 tumor-suppressor function. MDM4, an essential negative regulator of the P53 tumor suppressor, is frequently overexpressed in cancer cells that harbor a wild-type P53. MDM4 is a key regulator of p53, whose biological activities depend on both transcriptional activity and transcription-independent mitochondrial functions. MDM4 binds to p53 and blocks its transcriptional activity.

| 规格 | 价格 | 库存 | 数量 |
|---|---|---|---|
| 5 μg | ¥ 683 | 6-8日内发货 | |
| 10 μg | ¥ 1,130 | 6-8日内发货 | |
| 20 μg | ¥ 1,930 | 5日内发货 | |
| 50 μg | ¥ 4,430 | 5日内发货 |
| 生物活性 | Activity testing is in progress. It is theoretically active, but we cannot guarantee it. If you require protein activity, we recommend choosing the eukaryotic expression version first. |
| 产品描述 | MDM4 (MDM4 Regulator Of P53, also known as MDMX) is a Protein Coding gene. This gene encodes a nuclear protein that contains a p53 binding domain at the N-terminus and a RING finger domain at the C-terminus and shows structural similarity to p53-binding protein MDM2. MDM4 is a promising target for cancer therapy, as it is undetectable in most normal adult tissues but often upregulated in cancer cells to dampen p53 tumor-suppressor function. MDM4, an essential negative regulator of the P53 tumor suppressor, is frequently overexpressed in cancer cells that harbor a wild-type P53. MDM4 is a key regulator of p53, whose biological activities depend on both transcriptional activity and transcription-independent mitochondrial functions. MDM4 binds to p53 and blocks its transcriptional activity. |
| 种属 | Human |
| 表达系统 | E. coli |
| 标签 | N-His |
| 蛋白编号 | O15151-1 |
| 别名 | MRP1,MDMX,MDM4, p53 regulator,HDMX |
| 蛋白构建 | A DNA sequence encoding the human MDM4 (NP_002384.2) (Met1-Asp134) was expressed with a polyhistidine tag at the N-terminus. Predicted N terminal: His |
| 蛋白纯度 | > 90 % as determined by SDS-PAGE |
| 分子量 | 17 kDa (predicted); 19.4 kDa (reducing conditions) |
| 内毒素 | Please contact us for more information. |
| 蛋白性状 | Lyophilized powder |
| 缓冲液 | Lyophilized from a solution filtered through a 0.22 μm filter, containing PBS, pH 7.4. Typically, a mixture containing 5% to 8% trehalose, mannitol, and 0.01% Tween 80 is incorporated as a protective agent before lyophilization. |
| 复溶方法 | A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information. |
| 存储 | It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots. |
| 运输方式 | In general, Lyophilized powders are shipping with blue ice. |
| 研究背景 | MDM4 (MDM4 Regulator Of P53, also known as MDMX) is a Protein Coding gene. This gene encodes a nuclear protein that contains a p53 binding domain at the N-terminus and a RING finger domain at the C-terminus and shows structural similarity to p53-binding protein MDM2. MDM4 is a promising target for cancer therapy, as it is undetectable in most normal adult tissues but often upregulated in cancer cells to dampen p53 tumor-suppressor function. MDM4, an essential negative regulator of the P53 tumor suppressor, is frequently overexpressed in cancer cells that harbor a wild-type P53. MDM4 is a key regulator of p53, whose biological activities depend on both transcriptional activity and transcription-independent mitochondrial functions. MDM4 binds to p53 and blocks its transcriptional activity. |