ArticleMolecular and cellular biology2010
Mutational analysis of the poly(ADP-ribosyl)ation sites of the transcription factor CTCF provides an insight into the mechanism of its regulation by poly(ADP-ribosyl)ation.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 86 citations in OpenAlex.
- Re-establishment of TAD boundary organization during DNA replication.bioRxiv : the preprint server for biology · 2026Article
- Molecular Mimics: How Viral Genomes Dupe Their Host by Usurping CTCF to Establish Infection.Viruses · 2026Review
- Ectopic Recruitment of the CTCF N-Terminal Domain with Two Proximal Zinc-Finger Domains as a Tool for 3D Genome Engineering.International journal of molecular sciences · 2025Article
- PARP1 as an Epigenetic Modulator: Implications for the Regulation of Host-Viral Dynamics.Pathogens (Basel, Switzerland) · 2024Review
- Interplay between epigenetics and metabolism controls cancer stem cell plasticity.Frontiers in epigenetics and epigenomics · 2024Review
- Recent advances in chromosome capture techniques unraveling 3D genome architecture in germ cells, health, and disease.Functional & integrative genomics · 2023Review
- Three-Dimensional Chromatin Structure of the EBV Genome: A Crucial Factor in Viral Infection.Viruses · 2023Review
- Review
- DNA Methylation Malleability and Dysregulation in Cancer Progression: Understanding the Role of PARP1.Biomolecules · 2022Review
- PARP-1 regulates inflammasome activity by poly-ADP-ribosylation of NLRP3 and interaction with TXNIP in primary macrophages.Cellular and molecular life sciences : CMLS · 2022Article
- The three-dimensional structure of Epstein-Barr virus genome varies by latency type and is regulated by PARP1 enzymatic activity.Nature communications · 2022Article
- Review
- MyoD induces ARTD1 and nucleoplasmic poly-ADP-ribosylation during fibroblast to myoblast transdifferentiation.iScience · 2021Article
- Dynamic regulation of CTCF stability and sub-nuclear localization in response to stress.PLoS genetics · 2021Article
- CTCF as a boundary factor for cohesin-mediated loop extrusion: evidence for a multi-step mechanism.Nucleus (Austin, Tex.) · 2020Review
- Molecular basis of CTCF binding polarity in genome folding.Nature communications · 2020Article
- NPM1c impedes CTCF functions through cytoplasmic mislocalization in acute myeloid leukemia.Leukemia · 2020Article
- PARPs and ADP-ribosylation in RNA biology: from RNA expression and processing to protein translation and proteostasis.Genes & development · 2020Review
- CGGBP1 regulates CTCF occupancy at repeats.Epigenetics & chromatin · 2019Article
- The Role of PARPs in Inflammation-and Metabolic-Related Diseases: Molecular Mechanisms and Beyond.Cells · 2019Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Poly(ADP-ribosyl)ation of the conserved multifunctional transcription factor CTCF was previously identified as important to maintain CTCF insulator and chromatin barrier functions. However, the molecular mechanism of this regulation and also the necessity of this modification for other CTCF functions remain unknown. In this study, we identified potential sites of poly(ADP-ribosyl)ation within the N-terminal domain of CTCF and generated a mutant deficient in poly(ADP-ribosyl)ation. Using this CTCF mutant, we demonstrated the requirement of poly(ADP-ribosyl)ation for optimal CTCF function in transcriptional activation of the p19ARF promoter and inhibition of cell proliferation. By using a newly generated isogenic insulator reporter cell line, the CTCF insulator function at the mouse Igf2-H19 imprinting control region (ICR) was found to be compromised by the CTCF mutation. The association and simultaneous presence of PARP-1 and CTCF at the ICR, confirmed by single and serial chromatin immunoprecipitation assays, were found to be independent of CTCF poly(ADP-ribosyl)ation. These results suggest a model of CTCF regulation by poly(ADP-ribosyl)ation whereby CTCF and PARP-1 form functional complexes at sites along the DNA, producing a dynamic reversible modification of CTCF. By using bioinformatics tools, numerous sites of CTCF and PARP-1 colocalization were demonstrated, suggesting that such regulation of CTCF may take place at the genome level.
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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.