ArticleNature communications2017
USP26 functions as a negative regulator of cellular reprogramming by stabilising PRC1 complex components.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed.
- From Primary Cells to Organoids: Expanding the Biological Relevance of In Vitro Cellular Models.Cells · 2026Review
- The Potential Role of Deubiquitinating Enzymes (DUBs) in Male Fertility.Biomolecules · 2026Review
- Unravelling the impact of the chromobox proteins in human cancers.Cell death & disease · 2025Review
- A chromatin-focused CRISPR screen identifies USP22 as a barrier to somatic cell reprogramming.Communications biology · 2025Article
- USP26 Combats Age-Related Declines in Self-Renewal and Multipotent Differentiation of BMSC by Maintaining Mitochondrial Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The occurrence and development of induced pluripotent stem cells.Frontiers in genetics · 2024Review
- CBX4 contributes to radioresistance by regulating autophagic activity in esophageal squamous cell carcinoma.Annals of translational medicine · 2022Article
- Roles of ubiquitination in the crosstalk between tumors and the tumor microenvironment (Review).International journal of oncology · 2022Review
- The osteoprotective role of USP26 in coordinating bone formation and resorption.Cell death and differentiation · 2022Article
- USP26 promotes anaplastic thyroid cancer progression by stabilizing TAZ.Cell death & disease · 2022Article
- Discovery of Potent Peptidomimetic Antagonists for Heterochromatin Protein 1 Family Proteins.ACS omega · 2022Article
- Paternal USP26 mutations raise Klinefelter syndrome risk in the offspring of mice and humans.The EMBO journal · 2021Article
- Novel Mutations in X-Linked,Cells · 2021Article
- Deubiquitylases in developmental ubiquitin signaling and congenital diseases.Cell death and differentiation · 2021Review
- SNAIL1: Linking Tumor Metastasis to Immune Evasion.Frontiers in immunology · 2021Review
- SALL1 Modulates CBX4 Stability, Nuclear Bodies, and Regulation of Target Genes.Frontiers in cell and developmental biology · 2021Article
- Proteasomal degradation of polycomb-group protein CBX6 confers MMP-2 expression essential for mesothelioma invasion.Scientific reports · 2020Article
- Linc00668 Promotes Invasion and Stem Cell-Like Properties of Breast Cancer Cells by Interaction With SND1.Frontiers in oncology · 2020Article
- Reprogramming: identifying the mechanisms that safeguard cell identity.Development (Cambridge, England) · 2019Review
- Usp26 mutation in mice leads to defective spermatogenesis depending on genetic background.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Despite much progress in the comprehension of the complex process of somatic cell reprogramming, many questions regarding the molecular mechanism of regulation remain to be answered. At present, the knowledge on the negative regulation of reprogramming process is indeed poor in contrary to the identification of positive regulators. Here we report for the first time that ubiquitin-specific protease 26 negatively regulates somatic cell-reprogramming process by stabilizing chromobox (CBX)-containing proteins CBX4 and CBX6 of polycomb-repressive complex 1 through the removal of K48-linked polyubiquitination. Thus, accumulated CBX4 and CBX6 repress the expression of pluripotency genes, such as Sox2 and Nanog, through PRC1 complexes to ubiquitinate histone H2A at their promoters. In all, our findings have revealed an essential role for ubiquitin-specific protease 26 in cellular reprogramming through polycomb-repressive complex 1.The ubiquitin-proteasome system regulates cellular reprogramming by degradation of key pluripotency factors. Here the authors report that the post-translational regulation of PRC1 components CBX4 and CBX6 by ubiquitination influences reprogramming.
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