ArticleGenes & development2001
Tumor formation and inactivation of RIZ1, an Rb-binding member of a nuclear protein-methyltransferase superfamily.
Article in Genes & development, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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
73 citing papers in PubMed, 210 citations in OpenAlex.
- PRDM2-The Key Research Targets for the Development of Diseases in Various Systems.Biomolecules · 2025Review
- Maternal PRDM10 activates essential genes for oocyte-to-embryo transition.Nature communications · 2025Article
- Epigenetic Biomarkers and the Wnt/β-Catenin Pathway in Opisthorchis viverrini-associated Cholangiocarcinoma: A Scoping Review on Therapeutic Opportunities.PLoS neglected tropical diseases · 2024Article
- Tumor-suppressive functions of protein lysine methyltransferases.Experimental & molecular medicine · 2023Review
- Exploring the putative role of PRDM1 and PRDM2 transcripts as mediators of T lymphocyte activation.Journal of translational medicine · 2023Article
- The duality of PRDM proteins: epigenetic and structural perspectives.The FEBS journal · 2022Review
- Applying differential network analysis to longitudinal gene expression in response to perturbations.Frontiers in genetics · 2022Article
- Is There a Histone Code for Cellular Quiescence?Frontiers in cell and developmental biology · 2021Review
- PRDM15 is a key regulator of metabolism critical to sustain B-cell lymphomagenesis.Nature communications · 2020Article
- Multifaceted Role of PRDM Proteins in Human Cancer.International journal of molecular sciences · 2020Review
- Searching for a Putative Mechanism of RIZ2 Tumor-Promoting Function in Cancer Models.Frontiers in oncology · 2020Article
- New discoveries of mdig in the epigenetic regulation of cancers.Seminars in cancer biology · 2019Review
- Off to a Bad Start: Cancer Initiation by Pluripotency Regulator PRDM14.Trends in genetics : TIG · 2019Review
- Genome-wide promoter methylation of hairy cell leukemia.Blood advances · 2019Article
- Detection of Molecular Alterations in Taiwanese Patients with Medullary Thyroid Cancer Using Whole-Exome Sequencing.Endocrine pathology · 2018Article
- Genetic background influences susceptibility to chemotherapy-induced hematotoxicity.The pharmacogenomics journal · 2018Article
- Repression of Akt3 gene transcription by the tumor suppressor RIZ1.Scientific reports · 2018Article
- SomaticOncotarget · 2017Article
- CRISPR/Cas9-mediated deletion of lncRNA Gm26878 in the distant Foxf1 enhancer region.Mammalian genome : official journal of the International Mammalian Genome Society · 2017Article
- Writing, erasing and reading histone lysine methylations.Experimental & molecular medicine · 2017Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 9 institutions in 2 countries.
Funding
Abstract
The retinoblastoma protein-interacting zinc finger gene RIZ (PRDM2) is a member, by sequence homology, of a nuclear protein-methyltransferase (MTase) superfamily involved in chromatin-mediated gene expression. The gene produces two protein products, RIZ1 that contains a conserved MTase domain and RIZ2 that lacks the domain. RIZ1 gene expression is frequently silenced in human cancers, and the gene is also a common target of frameshift mutation in microsatellite-unstable cancers. We now report studies of mice with a targeted mutation in the RIZ1 locus. The mutation inactivates RIZ1 but not RIZ2. These RIZ1 mutant mice were viable and fertile but showed a high incidence of diffuse large B-cell lymphomas (DLBL) and a broad spectrum of unusual tumors. RIZ1 deficiency also accelerated tumorigenesis in p53 heterozygous mutant mice. Finally, several missense mutations of RIZ1 were found in human tumor tissues and cell lines; one of these was particularly common in human DLBL tumors. These missense mutations, as well as the previously described frameshift mutation, all mapped to the MTase functional domains. All abolished the capacity of RIZ1 to enhance estrogen receptor activation of transcription. These data suggest a direct link between tumor formation and the MTase domain of RIZ1 and describe for the first time a tumor susceptibility gene among methyltransferases.
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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.