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Mouse Anti-MDM4 Recombinant Antibody (CBFYM-1966) (CBMAB-M2141-FY)

This product is mouse antibody that recognizes MDM4. The antibody CBFYM-1966 can be used for immunoassay techniques such as: ELISA, WB, IHC, IF, ICC.
See all MDM4 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBFYM-1966
Antibody Isotype
IgG1
Application
ELISA, WB, IHC, IF, ICC

Basic Information

Immunogen
Recombinant fragment of human MDM4 expressed in E. coli
Specificity
Human
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Minichromosome Maintenance Complex Component 4
Introduction
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. Both proteins bind the p53 tumor suppressor protein and inhibit its activity, and have been shown to be overexpressed in a variety of human cancers. However, unlike MDM2 which degrades p53, this protein inhibits p53 by binding its transcriptional activation domain. This protein also interacts with MDM2 protein via the RING finger domain, and inhibits the latter's degradation. So this protein can reverse MDM2-targeted degradation of p53, while maintaining suppression of p53 transactivation and apoptotic functions. Alternatively spliced transcript variants encoding different isoforms have been noted for this gene.
Entrez Gene ID
UniProt ID
Alternative Names
MDM4, P53 Regulator; Mdm2-Like P53-Binding Protein; Protein Mdmx; MDMX; Mdm4, Transformed 3T3 Cell Double Minute 4, P53 Binding Protein (Mouse); Mouse Double Minute 4, Human Homolog Of; P53-Binding Protein; Double Minute 4, Human Homolog Of; P53-Binding Protein; Mdm4 P53 Binding Protein Homolog (Mouse); Mdm4 P53 Binding Protein Homolog
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.
Biological Process
Atrial septum development Source: BHF-UCL
Atrioventricular valve morphogenesis Source: BHF-UCL
Cellular response to hypoxia Source: UniProtKB
DNA damage response, signal transduction by p53 class mediator Source: UniProtKB
Endocardial cushion morphogenesis Source: BHF-UCL
Heart valve development Source: BHF-UCL
Negative regulation of apoptotic process Source: InterPro
Negative regulation of cell population proliferation Source: ProtInc
Negative regulation of protein catabolic process Source: UniProtKB
Negative regulation of transcription, DNA-templated Source: ComplexPortal
Negative regulation of transcription by RNA polymerase II Source: UniProtKB
Protein-containing complex assembly Source: UniProtKB
Protein stabilization Source: UniProtKB
Regulation of cell cycle Source: InterPro
Regulation of transcription by RNA polymerase II Source: GO_Central
Ventricular septum development Source: BHF-UCL
Cellular Location
Nucleus
Involvement in disease
Bone marrow failure syndrome 6 (BMFS6):
A form of bone marrow failure syndrome, a heterogeneous group of life-threatening disorders characterized by hematopoietic defects in association with a range of variable extra-hematopoietic manifestations. BMFS6 is an autosomal dominant form characterized by intermittent neutropenia, lymphopenia, or anemia associated with hypocellular bone marrow, and increased susceptibility to cancer.
PTM
Phosphorylated. Phosphorylation at Ser-367 promotes interaction with YWHAG and subsequent ubiquitination and degradation. Phosphorylation at Ser-342 also induces ubiquitination and degradation but to a lower extent.
Ubiquitinated and degraded by MDM2. Deubiquitination by USP2 on the other hand stabilizes the MDM4 protein.

Sanford, J. D., Yang, J., Han, J., Tollini, L. A., Jin, A., & Zhang, Y. (2021). MDMX is essential for the regulation of p53 protein levels in the absence of a functional MDM2 C-terminal tail. BMC Molecular and Cell Biology, 22, 1-9.

Wu, J., Lu, G., & Wang, X. (2021). MDM4 alternative splicing and implication in MDM4 targeted cancer therapies. American Journal of Cancer Research, 11(12), 5864.

Zhang, S., Lou, J., Li, Y., Zhou, F., Yan, Z., Lyu, X., & Zhao, Y. (2021). Recent progress and clinical development of inhibitors that block MDM4/p53 protein–protein interactions. Journal of Medicinal Chemistry, 64(15), 10621-10640.

Eskandari, M., Shi, Y., Liu, J., Albanese, J., Goel, S., Verma, A., & Wang, Y. (2021). The expression of MDM2, MDM4, p53 and p21 in myeloid neoplasms and the effect of MDM2/MDM4 dual inhibitor. Leukemia & Lymphoma, 62(1), 167-175.

Wohlberedt, K., Klusmann, I., Derevyanko, P. K., Henningsen, K., Choo, J. A. M. Y., Manzini, V., ... & Dobbelstein, M. (2020). Mdm4 supports DNA replication in a p53-independent fashion. Oncogene, 39(25), 4828-4843.

Liu, T., Zhang, H., Yi, S., Gu, L., & Zhou, M. (2019). Mutual regulation of MDM 4 and TOP 2A in cancer cell proliferation. Molecular oncology, 13(5), 1047-1058.

Haupt, S., Mejía-Hernández, J. O., Vijayakumaran, R., Keam, S. P., & Haupt, Y. (2019). The long and the short of it: the MDM4 tail so far. Journal of molecular cell biology, 11(3), 231-244.

Karki, A., Putra, J., Kim, S. S., Laquaglia, M. J., Perez‑Atayde, A. R., Sadri‑Vakili, G., & Vakili, K. (2019). MDM4 expression in fibrolamellar hepatocellular carcinoma. Oncology Reports, 42(4), 1487-1496.

Frosi, Y., Inoue, K., Ramlan, S. R., Lane, D. P., Watanabe, T., & Brown, C. J. (2019). Simultaneous measurement of p53: Mdm2 and p53: Mdm4 protein-protein interactions in whole cells using fluorescence labelled foci. Scientific Reports, 9(1), 17933.

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For research use only. Not intended for any clinical use.

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