ArticleMolecular and cellular biology2007
Functional analysis of the transcription repressor PLU-1/JARID1B.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 140 citations in OpenAlex.
- A KDM5 variant outside the catalytic Jumonji C domain disrupts demethylase activity and alters the proximity interactome.G3 (Bethesda, Md.) · 2026Article
- miR-770-5p regulates KDM5B and links its nuclear localization to HER2 signaling in trastuzumab-resistant breast cancer.Molecular and cellular biochemistry · 2026Article
- Design and characterization of G-quadruplex RNA aptamers reveal RNA-binding by KDM5 lysine demethylases.Computational and structural biotechnology journal · 2025Article
- Discovery and structural studies of histone demethylases.Frontiers in epigenetics and epigenomics · 2025Review
- The emerging roles of histone demethylases in cancers.Cancer metastasis reviews · 2024Review
- KDM5 family as therapeutic targets in breast cancer: Pathogenesis and therapeutic opportunities and challenges.Molecular cancer · 2024Review
- ARID3a from the ARID family: structure, role in autoimmune diseases and drug discovery.Acta pharmacologica Sinica · 2023Review
- A truncated and catalytically inactive isoform of KDM5B histone demethylase accumulates in breast cancer cells and regulates H3K4 tri-methylation and gene expression.Cancer gene therapy · 2023Article
- Proximity labeling reveals a new in vivo network of interactors for the histone demethylase KDM5.Epigenetics & chromatin · 2023Article
- Chromatin Sensing by the Auxiliary Domains of KDM5C Regulates Its Demethylase Activity and Is Disrupted by X-linked Intellectual Disability Mutations.Journal of molecular biology · 2023Article
- KDM5 Lysine Demethylases in Pathogenesis, from Basic Science Discovery to the Clinic.Advances in experimental medicine and biology · 2023Article
- Review
- Persister state-directed transitioning and vulnerability in melanoma.Nature communications · 2022Article
- Histone Methylases and Demethylases Regulating Antagonistic Methyl Marks: Changes Occurring in Cancer.Cells · 2022Review
- Functions and Interactions of Mammalian KDM5 Demethylases.Frontiers in genetics · 2022Review
- KDM5B protein expressed in viable and fertile ΔARID mice exhibit no demethylase activity.International journal of oncology · 2021Article
- CRISPR/Cas13d-mediated efficient KDM5B mRNA knockdown in porcine somatic cells and parthenogenetic embryos.Reproduction (Cambridge, England) · 2021Article
- The emerging role of KDM5A in human cancer.Journal of hematology & oncology · 2021Review
- The Role of H3K4 Trimethylation in CpG Islands Hypermethylation in Cancer.Biomolecules · 2021Review
- Review
18 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The PLU-1/JARID1B nuclear protein, which is upregulated in breast cancers, belongs to the ARID family of DNA binding proteins and has strong transcriptional repression activity. To identify the target genes regulated by PLU-1/JARID1B, we overexpressed or silenced the human PLU-1/JARID1B gene in human mammary epithelial cells by using adenovirus and RNA interference systems, respectively, and then applied microarray analysis to identify candidate genes. A total of 100 genes showed inversely correlated differential expression in the two systems. Most of the candidate genes were downregulated by the overexpression of PLU-1/JARID1B, including the MT genes, the tumor suppressor gene BRCA1, and genes involved in the regulation of the M phase of the mitotic cell cycle. Chromatin immunoprecipitation assays confirmed that the metallothionein 1H (MT1H), -1F, and -1X genes are direct transcriptional targets of PLU-1/JARID1B in vivo. Furthermore, the level of trimethyl H3K4 of the MT1H promoter was increased following silencing of PLU-1/JARID1B. Both the PLU-1/JARID1B protein and the ARID domain selectively bound CG-rich DNA. The GCACA/C motif, which is abundant in metallothionein promoters, was identified as a consensus binding sequence of the PLU-1/JARID1B ARID domain. As expected from the microarray data, cells overexpressing PLU-1/JARID1B have an impaired G(2)/M checkpoint. Our study provides insight into the molecular function of the breast cancer-associated transcriptional repressor PLU-1/JARID1B.
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