ArticleHuman molecular genetics2016
Mouse Dux is myotoxic and shares partial functional homology with its human paralog DUX4.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 53 citations in OpenAlex.
- TBP regulates transposable element expression in early mouse embryos.The EMBO journal · 2026Article
- Development of a DUX4-targeting antibody oligonucleotide conjugate as a therapy for FSHD.Nucleic acids research · 2026Article
- CRISPRa-mediated disentanglement of the Dux-MERVL axis in the 2C-like state, totipotency, and cell death.Science advances · 2025Article
- Three-dimensional tissue engineered skeletal muscle modelling facioscapulohumeral muscular dystrophy.Brain : a journal of neurology · 2025Article
- Article
- Deciphering Facioscapulohumeral Dystrophy in the clinical trials era: where are we now?Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2025Review
- The role(s) of NF-Y in development and differentiation.Cell death and differentiation · 2025Review
- The pluripotent-to-totipotent state transition in mESCs activates the intrinsic apoptotic pathway through DUX-induced DNA replication stress.Cellular and molecular life sciences : CMLS · 2024Article
- Challenges and Considerations of Preclinical Development for iPSC-Based Myogenic Cell Therapy.Cells · 2024Review
- PDGFRβ Activation Induced the Bovine Embryonic Genome Activation via Enhanced NFYA Nuclear Localization.International journal of molecular sciences · 2023Article
- Antagonism among DUX family members evolved from an ancestral toxic single homeodomain protein.iScience · 2023Article
- Post-Translational Modifications of the DUX4 Protein Impact Toxic Function in FSHD Cell Models.Annals of neurology · 2023Article
- Antagonism among DUX family members evolved from an ancestral toxic single homeodomain protein.bioRxiv : the preprint server for biology · 2023Article
- Genome architecture and totipotency: An intertwined relation during early embryonic development.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Article
- The evolution of DUX4 gene regulation and its implication for facioscapulohumeral muscular dystrophy.Biochimica et biophysica acta. Molecular basis of disease · 2022Review
- DUX: One Transcription Factor Controls 2-Cell-like Fate.International journal of molecular sciences · 2022Review
- Review
- Embryonic LTR retrotransposons supply promoter modules to somatic tissues.Genome research · 2021Article
- DNA crosslinking and recombination-activating genes 1/2 (RAG1/2) are required for oncogenic splicing in acute lymphoblastic leukemia.Cancer communications (London, England) · 2021Article
- CTCF is a barrier for 2C-like reprogramming.Nature communications · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
D4Z4 repeats are present in at least 11 different mammalian species, including humans and mice. Each repeat contains an open reading frame encoding a double homeodomain (DUX) family transcription factor. Aberrant expression of the D4Z4 ORF called DUX4 is associated with the pathogenesis of Facioscapulohumeral muscular dystrophy (FSHD). DUX4 is toxic to numerous cell types of different species, and over-expression caused dysmorphism and developmental arrest in frogs and zebrafish, embryonic lethality in transgenic mice, and lesions in mouse muscle. Because DUX4 is a primate-specific gene, questions have been raised about the biological relevance of over-expressing it in non-primate models, as DUX4 toxicity could be related to non-specific cellular stress induced by over-expressing a DUX family transcription factor in organisms that did not co-evolve its regulated transcriptional networks. We assessed toxic phenotypes of DUX family genes, including DUX4, DUX1, DUX5, DUXA, DUX4-s, Dux-bl and mouse Dux. We found that DUX proteins were not universally toxic, and only the mouse Dux gene caused similar toxic phenotypes as human DUX4. Using RNA-seq, we found that 80% of genes upregulated by Dux were similarly increased in DUX4-expressing cells. Moreover, 43% of Dux-responsive genes contained ChIP-seq binding sites for both Dux and DUX4, and both proteins had similar consensus binding site sequences. These results suggested DUX4 and Dux may regulate some common pathways, and despite diverging from a common progenitor under different selective pressures for millions of years, the two genes maintain partial functional homology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.