Evidence map›Paper›PMID 29128342›Full record

ReviewPharmacology & therapeutics2018

Readers of DNA methylation, the MBD family as potential therapeutic targets.

Gordon D Ginder, David C Williams

Erratum issuedAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.8field-weighted citation impact, top 9% of its field
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

50 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024
    Review
  14. Prognostic Significance ofPhenomics (Cham, Switzerland) · 2024
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. MBD2a-NuRD binds to the methylated γ-globin gene promoter and uniquely forms a complex required for silencing of HbF expression.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Gordon D GinderDepartment of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, VA 23298, United States; Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA 23298, United States; Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298, United States. Electronic address: gdginder@vcu.edu.
David C WilliamsDepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States. Electronic address: david_willjr@med.unc.edu.
University of North Carolina at Chapel Hill · USVirginia Commonwealth University · US

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Kim Felder Rhoads · 1985 to 2026
$51.0M
GLOBIN GENE REGULATION DURING ERYTHROID DIFFERENTIATIONR01DK029902 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI GINDER, GORDON D · 1986 to 2010
$2.5M
Structural and functional diversity of the methyl-binding domain protein familyR01GM098264 · NIGMS · VIRGINIA COMMONWEALTH UNIVERSITY · PI WILLIAMS, DAVID COLLIN · 2012 to 2016
$1.4M
Regulation of Globin Gene Expression In Erythroid Differentiation & DevelopmentR56DK029902 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI GINDER, GORDON D · 2012 to 2012
$135k
NCI NIH HHS P30 CA016059NIDDK NIH HHS R01 DK029902NIDDK NIH HHS R56 DK029902NIGMS NIH HHS R01 GM098264
6 · The paper itself

Abstract

DNA methylation represents a fundamental epigenetic modification that regulates chromatin architecture and gene transcription. Many diseases, including cancer, show aberrant methylation patterns that contribute to the disease phenotype. DNA methylation inhibitors have been used to block methylation dependent gene silencing to treat hematopoietic neoplasms and to restore expression of developmentally silenced genes. However, these inhibitors disrupt methylation globally and show significant off-target toxicities. As an alternative approach, we have been studying readers of DNA methylation, the 5-methylcytosine binding domain family of proteins, as potential therapeutic targets to restore expression of aberrantly and developmentally methylated and silenced genes. In this review, we discuss the role of DNA methylation in gene regulation and cancer development, the structure and function of the 5-methylcytosine binding domain family of proteins, and the possibility of targeting the complexes these proteins form to treat human disease.

Indexed as

DNA MethylationAnimalsDNA-Binding ProteinsHumansModels, MolecularMolecular Targeted TherapyNeoplasmsDNA-Binding Proteins5-Methylcytosine binding domainChromatinDNA methylationGene regulationNuRD

Identifiers

PMID29128342
PMCPMC6438182
OpenAlexW2768049487

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.