ArticleNucleic acids research2010
The tumor suppressor, parafibromin, mediates histone H3 K9 methylation for cyclin D1 repression.
Article in Nucleic acids research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 84 citations in OpenAlex.
- Dynamic regulation of H3K9 modifications in cancer: pathogenesis and targeted therapies.Biomarker research · 2026Review
- CDC73 suppresses lung adenocarcinoma via the PTEN/AKT pathway and exhibits biomarker and functional potential in extracellular vesicles.Cell death discovery · 2026Article
- Evolutionary analysis of transcription elongation factors reveals conserved and lineage-specific regulatory domains.PLoS biology · 2026Article
- Parathyroid Carcinoma: From Molecular Pathogenesis and Diagnostic Biomarkers to Targeted Therapeutics.International journal of molecular sciences · 2026Review
- Genetic and pharmaceutical manipulation of H3K9 methyltransferase Suv39h1 promotes liver regeneration by unleashing HMGB2 transcription.Experimental & molecular medicine · 2026Article
- Evolutionary conservation and innovations of RNA polymerase II transcription elongation factors.bioRxiv : the preprint server for biology · 2026Article
- Article
- Genetics of hereditary forms of primary hyperparathyroidism.Hormones (Athens, Greece) · 2024Review
- Tyrosine phosphataseFrontiers in immunology · 2024Review
- SUV39H1 is a novel biomarker targeting oxidative phosphorylation in hepatitis B virus-associated hepatocellular carcinoma.BMC cancer · 2023Article
- Phenotypic Profiling and Molecular Mechanisms in Hyperparathyroidism-jaw Tumor Syndrome.The Journal of clinical endocrinology and metabolism · 2023Article
- Writers and readers of H3K9me2 form distinct protein networks during the cell cycle that include candidates for H3K9 mimicry.Bioscience reports · 2023Article
- Article
- The clinicopathological and prognostic significances of CDC73 expression in breast cancer: A pathological and bioinformatics analysis.Histology and histopathology · 2023Article
- Parafibromin governs cell polarity and centrosome assembly in Drosophila neural stem cells.PLoS biology · 2022Article
- Immunohistochemical Profile of Parathyroid Tumours: A Comprehensive Review.International journal of molecular sciences · 2022Review
- USP37 Deubiquitinates CDC73 in HPT-JT Syndrome.International journal of molecular sciences · 2022Article
- UBR5 targets tumor suppressor CDC73 proteolytically to promote aggressive breast cancer.Cell death & disease · 2022Article
- Overview of the 2022 WHO Classification of Parathyroid Tumors.Endocrine pathology · 2022Review
- SUV39H1 regulates corneal epithelial wound healing via H3K9me3-mediated repression of p27.Eye and vision (London, England) · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parafibromin, a component of the RNA polymerase II-associated PAF1 complex, is a tumor suppressor linked to hyperparathyroidism-jaw tumor syndrome and sporadic parathyroid carcinoma. Parafibromin induces cell cycle arrest by repressing cyclin D1 via an unknown mechanism. Here, we show that parafibromin interacts with the histone methyltransferase, SUV39H1, and functions as a transcriptional repressor. The central region (128-227 amino acids) of parafibromin is important for both the interaction with SUV39H1 and transcriptional repression. Parafibromin associated with the promoter and coding regions of cyclin D1 and was required for the recruitment of SUV39H1 and the induction of H3 K9 methylation but not H3 K4 methylation. RNA interference analysis showed that SUV39H1 was critical for cyclin D1 repression. These data suggest that parafibromin plays an unexpected role as a repressor in addition to its widely known activity associated with transcriptional activation. Parafibromin as a part of the PAF1 complex might downregulate cyclin D1 expression by integrating repressive H3 K9 methylation during transcription.
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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.