HdmX/MDM4 Antibody
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, IP |
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Primary Accession | O15151 |
Reactivity | Human |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 54864 Da |
Gene ID | 4194 |
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Application & Usage | Western blotting (1:500 – 1:1500) and Immunoprecipitation. MCF7 cell lysate can be used as a positive control. However, the optimal concentrations should be determined individually. The antibody recognizes the HdmX/MDM4 of human origin. Reactivity to other species has not been tested. |
Other Names | HdmX, MdmX, MDM4, homolog of mouse double minute 4 protein |
Target/Specificity | HdmX/MDM4 |
Antibody Form | Liquid |
Appearance | Colorless liquid |
Formulation | 100 µl affinity purified rabbit polyclonal antibody in phosphate-buffered saline (PBS) containing 30% glycerol, 1% BSA and 0.02% thimerosal. |
Handling | The antibody solution should be gently mixed before use. |
Reconstitution & Storage | -20 °C |
Background Descriptions | |
Precautions | HdmX/MDM4 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | MDM4 |
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Synonyms | MDMX |
Function | Along with MDM2, contributes to TP53 regulation (PubMed:32300648). Inhibits p53/TP53- and TP73/p73-mediated cell cycle arrest and apoptosis by binding its transcriptional activation domain. Inhibits degradation of MDM2. Can reverse MDM2-targeted degradation of TP53 while maintaining suppression of TP53 transactivation and apoptotic functions. |
Cellular Location | Nucleus. |
Tissue Location | Expressed in all tissues tested with high levels in thymus |
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Provided below are standard protocols that you may find useful for product applications.
Background
The MDM2 protein is the primary regulator of p53 protein stability. MDMX is an MDM2-related protein that inhibits MDM2-mediated degradation of p53 via distinct associations with MDM2. The gene that encodes MDMX (also designated MDM4) is a target for amplification in malignant gliomas. ARF interacts with MDMX to sequester MDMX within the nucleolus. This sequestration of MDMX by ARF results in an increase in p53 transactivation. In addition, expression of MDMX can reverse MDM2-targeted degradation of p53 while maintaining suppression of p53 transactivation. Like MDM2, MDMX also binds p73 and stabilizes the level of p73. Therefore, in striking contrast to p53, the half-life of p73 is increased by binding to MDM2.
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