ArticleOncogene2008
The transcriptional repressor NIPP1 is an essential player in EZH2-mediated gene silencing.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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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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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
58 citing papers in PubMed, 78 citations in OpenAlex.
- Trial
- Colorectal cancer co-opts an epidermal wound healing program during metastasis to generate disseminated tumor cells.Nature communications · 2026Article
- Epigenetic regulation of NDGA and its synergistic inhibition with EZH2 inhibitors in prostate cancer via NRP1.Acta pharmacologica Sinica · 2026Article
- Disordered DNA methylation leads to targetable transcriptional plasticity in ATRT.Acta neuropathologica communications · 2025Article
- AI-Driven Variant Annotation for Precision Oncology in Breast Cancer.Clinical and translational science · 2025Article
- Developmental stage and cellular context determine oncogenic and molecular outcomes ofBlood neoplasia · 2025Article
- HDAC7 induction combined with standard-of-care chemotherapy provides a therapeutic advantage in t(4;11) infant B-cell acute lymphoblastic leukemia.Biomarker research · 2025Article
- Article
- Sut-6/NIPP1 modulates tau toxicity.Human molecular genetics · 2023Article
- Combating castration-resistant prostate cancer by co-targeting the epigenetic regulators EZH2 and HDAC.PLoS biology · 2023Article
- Exploration of Tumor Biopsy Gene Signatures to Understand the Role of the Tumor Microenvironment in Outcomes to Lisocabtagene Maraleucel.Molecular cancer therapeutics · 2023Article
- Shaking up the silence: consequences of HMGN1 antagonizing PRC2 in the Down syndrome brain.Epigenetics & chromatin · 2022Review
- Targeting BMI-1 in B cells restores effective humoral immune responses and controls chronic viral infection.Nature immunology · 2022Article
- FUS-DDIT3 Fusion Oncoprotein Expression Affects JAK-STAT Signaling in Myxoid Liposarcoma.Frontiers in oncology · 2022Article
- Multi-omics analysis identifies therapeutic vulnerabilities in triple-negative breast cancer subtypes.Nature communications · 2021Article
- Somatic driver mutation prevalence in 1844 prostate cancers identifies ZNRF3 loss as a predictor of metastatic relapse.Nature communications · 2021Article
- PP1 regulatory subunit NIPP1 regulates transcription of E2F1 target genes following DNA damage.Cancer science · 2021Article
- Cell-penetrating, antioxidant SELENOT mimetic protects dopaminergic neurons and ameliorates motor dysfunction in Parkinson's disease animal models.Redox biology · 2021Article
- Implication of EZH2 in the Pro-Proliferative and Apoptosis-Resistant Phenotype of Pulmonary Artery Smooth Muscle Cells in PAH: A Transcriptomic and Proteomic Approach.International journal of molecular sciences · 2021Article
- Single-cell transcriptional changes associated with drug tolerance and response to combination therapies in cancer.Nature communications · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EZH2 is a Polycomb group (PcG) protein that promotes the late-stage development of cancer by silencing a specific set of genes, at least in part through trimethylation of associated histone H3 on Lys 27 (H3K27). Nuclear inhibitor of protein phosphatase-1 (NIPP1) is a ubiquitously expressed transcriptional repressor that has binding sites for the EZH2 interactor EED. Here, we examine the contribution of NIPP1 to EZH2-mediated gene silencing. Studies on NIPP1-deficient cells disclose a widespread and essential role of NIPP1 in the trimethylation of H3K27 by EZH2, not only in the onset of this trimethylation during embryonic development, but also in the maintenance of this repressive mark in proliferating cells. Consistent with this notion, EZH2 and NIPP1 silence a common set of genes, as revealed by gene-expression profiling, and NIPP1 is associated with established Polycomb target genes and with genomic regions that are enriched in Polycomb targets. Furthermore, most NIPP1 target genes are trimethylated on H3K27 and the knockdown of either NIPP1 or EZH2 is often associated with a loss of this modification. Our data reveal that NIPP1 is required for the global trimethylation of H3K27 and is implicated in gene silencing by EZH2.
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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.