Evidence map›Paper›PMID 40089655›Full record

ReviewMolecular biology reports2025

Versatile functions of methyl-CpG-binding domain 2 (MBD2) in cellular characteristics and differentiation.

Rabia Tuana Lekesiz, Kasım Kağan Koca, Gizem Kugu, Zihni Onur Çalışkaner

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
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

4 authors.

Rabia Tuana LekesizMolecular Biology and Genetics, Biruni University, Istanbul, Turkey.
Kasım Kağan Koca *Molecular Biology and Genetics, Gebze Technical University, Kocaeli, Turkey.
Gizem Kugu *Molecular Biology and Genetics, Gebze Technical University, Kocaeli, Turkey.
Zihni Onur ÇalışkanerMolecular Biology and Genetics, Biruni University, Istanbul, Turkey. zcaliskaner@biruni.edu.tr.

Funding

Türkiye Sağlık Enstitüleri Başkanlığı 2022-B-02-22387
6 · The paper itself

Abstract

Cellular differentiation is a vital process that results in cell specialization and functionalization, synchronized with the development and growth in multicellular organisms. Any fault in this process can bring about the emergence of various diseases. Gene expression controls cellular differentiation, but various epigenetic mechanisms play a pivotal role as well. For instance, DNA methylation and combined histone modifications, such as histone acetylation/deacetylation, are crucial in cellular differentiation. Methyl-CpG-Binding Domain 2 (MBD2), a highly conserved member of the MBD protein family, is considered a reader of DNA methylation and drives the crosstalk between DNA methylation and histone deacetylation. It can functionally recruit the nucleosome remodeling and deacetylase (NuRD) complex to the CpG-methylated promoters of the genes, which will be silenced during the cell fate determination. This review focuses on the cell-specific functions of MBD2 isoforms (MBD2a, MBD2b, and MBD2c(t)) in cellular differentiation, reprogramming, and the immune system. Furthermore, the relevance between MBD2 and certain cancers was discussed for the first time in this paper. Thus, we provide a comprehensive review about the significance of MBD2 in various cellular mechanisms.

Indexed as

Cell DifferentiationDNA-Binding ProteinsAnimalsCpG IslandsDNA MethylationEpigenesis, GeneticHistonesHumansDNA-Binding ProteinsHistonesMBD2 proteinMBD2 protein, humanDifferentiationDNA methylationEpigeneticsGametogenesisStem cellsTumorigenesis

Identifiers

What OpenQuestion holds

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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.