Ask about this productRelated genes to: MDM4 antibody
- Gene:
- MDM4 NIH gene
- Name:
- MDM4 regulator of p53
- Previous symbol:
- -
- Synonyms:
- MDMX, HDMX
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-09-05
- Date modifiied:
- 2019-01-25
Related products to: MDM4 antibody
Related articles to: MDM4 antibody
- - Source: PubMed
Publication date: 2026/04/27
Shuai XueqianSun YaoqiLi JialeGao YuanCheng ZhongpingLiu Shupeng - Detecting chromosomal copy-number alterations together with protein-defined cell states in intact tissue is critical for understanding early clonal evolution and microenvironmental interactions in cancer. We developed ORION-FISH, which integrates high-plex tissue imaging with a morphology-preserving DNA-FISH workflow and single-cell registration, yielding measurements concordant with clinical FISH. In High Grade Serous Ovarian Carcinoma (HGSOC), ORION-FISH recapitulated known chromosomal changes while revealing subclonal heterogeneity missed by targeted sequencing. Applied to serous tubal intraepithelial carcinomas (STICs), precursors of HGSOC, ORION-FISH identified intermixed epithelial cells with MYC or CCNE1 copy-number gains, as well as concurrent alterations associated with distinct immune microenvironments. In addition, epithelial cells with MYC and CCNE1 copy-number gains were detected in morphologically normal fallopian tube epithelium, along with rare MDM4 increases across epithelial lineages. Together, ORION-FISH provides a framework linking chromosomal copy number states to protein-defined phenotypes within preserved tissue architecture, enabling context-aware interrogation of early copy-number diversification at single-cell resolution. - Source: PubMed
Publication date: 2026/04/18
Kader TanjinaChen Yu-AnHug Clemens BLin Jia-RenMuhlich Jeremy LCoy ShannonJung EuihyeSchwartz Lauren EFazio ThomasChiu CrystalRyall Scott TDrescher Charles WSorger Peter KDrapkin RonnySantagata Sandro - Long non-coding RNAs (lncRNAs) can function as competing endogenous RNAs (ceRNAs) that rewire post-transcriptional regulation in glioblastoma (GBM). Previous GBM studies have focused on either single lncRNA ceRNA axis in isolation or used predictions with small patient cohorts (< 200). In this study, we integrated RNA-seq data from 372 TCGA-GBM tumors, 5 matched adjacent TCGA-normal brain and 2 931 GTEx-normal brain (n = 3 308) samples to build an experimentally informed ceRNA atlas. Limma-voom differential analysis, intersection with 2 experimentally supported interaction databases (ENCORI and miRTarBase) distilled 517 high-confidence lncRNA-miRNA-mRNA triplets. Twelve hub lncRNAs coordinated 3 downregulated miRNAs and 262 target mRNAs enriched for cell-cycle, p53 signaling and homologous recombination pathways. Two co-expressed hubs, and , were significantly over-expressed in GBM tumors in comparison with normal brain tissue and independently predicted poor overall survival (log-rank < .01). Their shared 25 targets include oncogenic , and mRNAs, underscoring the redundant regulation of oncogenic pathways, suggesting the need to explore combination lncRNA inhibition strategies. This population-scale analysis prioritizes and for functional interrogation and offers a framework for exploring biomarkers and RNA-targeted strategies in GBM. - Source: PubMed
Publication date: 2026/04/09
Rana ZohaibGrans Joke - MDM4 (Murine Double Minute 4), also known as MDMX, is a crucial negative regulator of the tumor suppressor p53. MDM4 heterodimerizes with MDM2 to enhance MDM2-mediated ubiquitination and degradation of p53, thereby promoting tumorigenesis. Beyond its canonical role in inhibiting p53 activity, recent studies have revealed diverse p53-independent functions. MDM4 interacts with various proteins, including p73, E2F1, casein kinase 1α, PPARα, and TRIM21 to regulate cell cycle progression, β-catenin-mediated pre-leukemic progression, and ferroptosis independent of p53. In addition, MDM4 functions independently of both p53 and MDM2 by interacting with proteins, such as SMAD family members 3/4, retinoblastoma protein (pRB), p21, Nbs1 (also known as Nibrin), mTOR complex 1 (mTORC1), and the Polycomb Repressive Complexes (PRCs) complex, to control cell proliferation and survival, as well as protein degradation, double-strand break (DSB) repair, and replication fork progression. Intriguingly, multiple studies suggest that MDM4 exhibits oncogenic activity independent of p53; however, other reports highlight a potential tumor-suppressive role for MDM4 in the absence of p53. Thus, MDM4's functions extend well beyond the canonical p53-MDM2 axis. A deeper understanding of MDM4 biology may facilitate the development of novel targeted therapies for various cancers. - Source: PubMed
Publication date: 2026/03/25
Thapa DipeshSt John AllisonParrales AlejandroRanjan AtulIwakuma Tomoo - Targeted therapies are reshaping oncology by enabling treatment selection based on actionable molecular alterations, improving precision, and reducing unnecessary toxicity. This review provides an up-to-date overview of current targeted treatment modalities and the medicinal chemistry principles that support their discovery and optimization. We synthesize evidence on small-molecule and biologic strategies spanning receptor and non-receptor kinases and their major signaling axes (PI3K-AKT-mTOR and RAS-RAF-MEK-ERK), apoptosis regulation (BCL-2 family), DNA repair via poly(ADP-ribose) polymerase (PARP) inhibition, and epigenetic or metabolic targets including histone deacetylases (HDACs), bromodomain and extra-terminal proteins (BET), and mutant isocitrate dehydrogenases (IDH1/2). Across these areas, we summarize recurrent resistance mechanisms and the rationale for combination or sequential approaches. Biologic targeted therapy is discussed in parallel, including immune checkpoint blockade, antibody-drug conjugates, bispecific antibodies (BsAb), and cell therapies such as chimeric antigen receptor T cells, with emphasis on biomarker-guided patient stratification. Finally, we outline emerging directions beyond canonical nodes, including modulation of the p53-MDM2/MDM4 axis, ferroptosis control through AIFM2/FSP1, and innate immune pathways such as CD47-SIRPa and the stimulator of interferon genes (STING). Overall, the field is shifting from single-target inhibition toward integrated strategies that combine precise molecular targeting with an understanding of signaling network dynamics, resistance evolution, and therapeutic vulnerabilities. - Source: PubMed
Publication date: 2026/04/03
Giercuszkiewicz-Haśnik KlaudiaMorak-Młodawska BeataJeleń Małgorzata