Evidence map›Paper›PMID 25753672›Full record

ArticleNucleic acids research2015

Dissecting the behavior and function of MBD3 in DNA methylation homeostasis by single-molecule spectroscopy and microscopy.

Yi Cui, Joseph Irudayaraj

Abstract read
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed.

  1. Review
  2. Development and validation of anTranslational cancer research · 2025
    Article
  3. Modeling DNA methyltransferase function to predict epigenetic correlation patterns in healthy and cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Osteosarcoma mechanobiology and therapeutic targets.British journal of pharmacology · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Adult Neural Stem Cell Multipotency and Differentiation Are Directed by the Methyl-CpG-Binding Protein MBD1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. MBD3 mediates epigenetic regulation on EPAS1 promoter in cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Yi CuiDepartment of Agricultural and Biological Engineering, 225 S. University Street, Purdue University, West Lafayette, IN 47907, USA Bindley Bioscience Center, 1203 W. State Street, Purdue University, West Lafayette, IN 47907, USA.
Joseph IrudayarajDepartment of Agricultural and Biological Engineering, 225 S. University Street, Purdue University, West Lafayette, IN 47907, USA Bindley Bioscience Center, 1203 W. State Street, Purdue University, West Lafayette, IN 47907, USA josephi@purdue.edu.

Funding

Transgenic Mouse Core Facility Shared Resource (TMCF-SR)P30CA023168 · NCI · PURDUE UNIVERSITY WEST LAFAYETTE · PI John Tesmer · 1985 to 2026
$43.4M
NCI NIH HHS P30CA023168
6 · The paper itself

Abstract

The detailed mechanism for DNA methylation homeostasis relies on an intricate regulatory network with a possible contribution from methyl-CpG-binding domain protein 3 (MBD3). In this study we examine the single-molecule behavior of MBD3 and its functional implication in balancing the activity of DNA methyltransferases (DNMTs). Besides a localization tendency to DNA demethylating sites, MBD3 experiences a concurrent transcription with DNMTs in cell cycle. Fluorescence lifetime correlation spectroscopy (FLCS) and photon counting histogram (PCH) were applied to characterize the chromatin binding kinetics and stoichiometry of MBD3 in different cell phases. In the G1-phase, MBD3, in the context of the Mi-2/NuRD (nucleosome remodeling deacetylase) complex, could adopt a salt-dependent homodimeric association with its target epigenomic loci. Along with cell cycle progression, utilizing fluorescence lifetime imaging microscopy-based Förster resonance energy transfer (FLIM-FRET) we revealed that a proportion of MBD3 and MBD2 would co-localize with DNMT1 during DNA maintenance methylation, providing a proofreading and protective mechanism against a possible excessive methylation by DNMT1. In accordance with our hypothesis, insufficient MBD3 induced by small interfering RNA (siRNA) was found to result in a global DNA hypermethylation as well as increased methylation in the promoter CpG islands (CGIs) of a number of cell cycle related genes.

Indexed as

DNA MethylationBinding SitesCell CycleCpG IslandsDNA-Binding ProteinsDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA Modification MethylasesFluorescence Resonance Energy TransferHeLa CellsHumansKineticsMi-2 Nucleosome Remodeling and Deacetylase ComplexMicroscopy, FluorescenceModels, MolecularPromoter Regions, GeneticDNA-Binding ProteinsDNA (Cytosine-5-)-Methyltransferase 1DNA (Cytosine-5-)-MethyltransferasesDNA Modification MethylasesDNMT1 protein, humanMBD2 protein, humanMBD3 protein, humanMi-2 Nucleosome Remodeling and Deacetylase ComplexRecombinant Fusion ProteinsRNA, Small Interfering

Identifiers

PMID25753672
PMCPMC4381056

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Registered trials

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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.