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Mouse Monoclonal MDM4 Antibody

  • 中文名: MDM4抗体
  • 别    名: HDMX; MDMX; MRP1; MDM4
货号: IPD20247
Price: ¥1280
数量:
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验证与应用

应用及物种
WB 咨询技术 Human,Mouse,Rat
IF 咨询技术 Human,Mouse,Rat
IHC 1/200 - 1/1000 Human,Mouse,Rat
ICC 1/200 - 1/1000 Human,Mouse,Rat
FCM 咨询技术 Human,Mouse,Rat
Elisa 1/10000 Human,Mouse,Rat

产品详情

参考文献

以下是关于MDM4抗体的3篇参考文献及其简要摘要:

1. **"MDMX: a novel p53-binding protein with some functional properties of MDM2"**

- **作者**: Shvarts, A. et al.

- **摘要**: 该研究首次克隆并鉴定了MDMX(后称MDM4),证明其通过直接结合p53抑制其转录活性。文中使用特异性抗体验证MDM4与p53的相互作用,并发现其在正常组织和肿瘤中的差异性表达,为后续靶向治疗研究奠定基础。

2. **"Targeting MDM4 in Cancer: A New Therapeutic Opportunity"**

- **作者**: Wade, M. & Wahl, G.M.

- **摘要**: 文章综述了MDM4在p53调控和肿瘤发生中的作用,强调开发靶向MDM4的抑制剂和抗体的重要性。作者提到利用抗体阻断MDM4-p53结合可恢复p53的抑癌功能,为癌症治疗提供新策略。

3. **"Restoration of p53 Function in MDM4-Overexpressing Tumors by Selective MDM4 Antagonists"**

- **作者**: Bernal, F. et al.

- **摘要**: 研究团队开发了一种针对MDM4的小分子拮抗剂及特异性抗体,证明其在MDM4高表达的癌细胞中能有效释放p53活性,诱导凋亡。抗体被用于体外和体内模型中验证MDM4的靶向效果。

如需具体文献来源,建议通过PubMed或Sci-Hub输入标题/作者进一步检索全文。

背景信息

The MDM4 (Murine Double Minute 4) protein, also known as MDMX, is a critical regulator of the tumor suppressor p53. It belongs to the MDM family, alongside MDM2. and functions primarily by binding to p53 to inhibit its transcriptional activity, thereby promoting cell survival under normal conditions. Unlike MDM2. which acts as an E3 ubiquitin ligase to degrade p53. MDM4 predominantly suppresses p53 through direct interaction, though it can also collaborate with MDM2 to enhance p53 inactivation. Dysregulation of MDM4 is implicated in cancer, as its overexpression in tumors silences p53-mediated apoptosis and cell cycle arrest, enabling uncontrolled proliferation.

MDM4 antibodies are essential tools for studying its expression, localization, and interaction with p53 or MDM2 in cancer research. These antibodies enable detection of MDM4 in tissues or cell lines via techniques like Western blot, immunohistochemistry, or immunofluorescence. Additionally, therapeutic antibodies targeting MDM4 are being explored to reactivate p53 in cancers retaining wild-type p53. Challenges include distinguishing MDM4 isoforms and minimizing cross-reactivity with MDM2 due to structural similarities. Current studies focus on developing small-molecule inhibitors or gene-silencing strategies to disrupt MDM4-p53 binding, offering potential for combination therapies with MDM2 inhibitors or chemotherapeutics. Despite preclinical promise, clinical translation remains in early stages, necessitating further research into tissue-specific MDM4 roles and resistance mechanisms.

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