ReviewFrontiers in genetics2016
Emerging Molecular and Biological Functions of MBD2, a Reader of DNA Methylation.
Review in Frontiers in genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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.
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.
Who cites it
57 citing papers in PubMed, 100 citations in OpenAlex.
- MBD2 suppresses SFRP1 expression and promotes colorectal cancer development by blocking MED19 binding to its methylated promoter.Cancer biology & therapy · 2026Article
- Gene regulatory mechanisms downstream of DNA methylation.Nature reviews. Genetics · 2026Review
- Glutamate-induced nuclear translocation of PYK2 in hippocampal neurons, interaction with MBD2, and role in cell death in a model of epilepsy.Cell death & disease · 2026Article
- The PKA/MBD2 Axis Transcriptionally Represses INPP5A to Modulate PI3K/Akt Signaling and Accelerate Pituitary Tumorigenesis.CNS neuroscience & therapeutics · 2026Article
- A New Complexity Layer: DNA Methylation and the Predictive Impact of Epigenetic Tests.International journal of molecular sciences · 2026Review
- Loss of MBD2 is associated with tumor growth in small intestinal neuroendocrine tumors.Endocrine connections · 2025Article
- Structural and Functional Studies on Key Epigenetic Regulators in Asthma.Biomolecules · 2025Review
- The role of MBD2 in immune cell development, function, and autoimmune diseases.Cell death discovery · 2025Review
- Uncovering the Molecular Interactions Underlying MBD2 and MBD3 Phase Separation.The journal of physical chemistry. B · 2025Article
- MBD2 promotes B cell differentiation and BCR signaling in systemic lupus erythematosus by regulating the LEF-1-PTEN-PI3K axis.Cell death & disease · 2025Article
- Targeting redox-sensitive MBD2-NuRD condensate in cancer cells.Nature cell biology · 2025Article
- Versatile functions of methyl-CpG-binding domain 2 (MBD2) in cellular characteristics and differentiation.Molecular biology reports · 2025Review
- Leveraging epigenetic aberrations in the pathogenesis of endometriosis: from DNA methylation to non-coding RNAs.Frontiers in genetics · 2025Review
- MBD2 regulates the progression and chemoresistance of cholangiocarcinoma through interaction with WDR5.Journal of experimental & clinical cancer research : CR · 2024Article
- Mechanistic model for epigenetic maintenance by methyl-CpG-binding domain proteins.bioRxiv : the preprint server for biology · 2024Article
- Article
- Article
- Methyl-CpG binding domain protein 2 (Mbd2) drives breast cancer progression through the modulation of epithelial-to-mesenchymal transition.Experimental & molecular medicine · 2024Article
- Reader-Effectors as Actuators of Epigenome Editing.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Epigenetic Dysregulation in Endometriosis: Implications for Pathophysiology and Therapeutics.Endocrine reviews · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA methylation is an epigenetic mark that is essential for many biological processes and is linked to diseases such as cancer. Methylation is usually associated with transcriptional silencing, but new research has challenged this model. Both transcriptional activation and repression have recently been found to be associated with DNA methylation in a context-specific manner. How DNA methylation patterns are interpreted into different functional output remains poorly understood. One mechanism involves the protein 'readers' of methylation, which includes the methyl-CpG binding domain (MBD) family of proteins. This review examines the molecular and biological functions of MBD2, which binds to CpG methylation and is an integral part of the nucleosome remodeling and histone deacetylation (NuRD) complex. MBD2 has been linked to immune system function and tumorigenesis, yet little is known about its functions in vivo. Recent studies have found the MBD2 protein is ubiquitously expressed, with relatively high levels in the lung, liver, and colon. Mbd2 null mice surprisingly show relatively mild phenotypes compared to mice with loss of function of other MBD proteins. This evidence has previously been interpreted as functional redundancy between the MBD proteins. Here, we examine and contextualize research that suggests MBD2 has unique properties and functions among the MBD proteins. These functions translate to recently described roles in the development and differentiation of multiple cell lineages, including pluripotent stem cells and various cell types of the immune system, as well as in tumorigenesis. We also consider possible models for the dynamic interactions between MBD2 and NuRD in different tissues in vivo. The functions of MBD2 may have direct therapeutic implications for several areas of human disease, including autoimmune conditions and cancer, in addition to providing insights into the actions of NuRD and chromatin regulation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.