ArticleMolecular and cellular biology2000
Active repression of methylated genes by the chromosomal protein MBD1.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 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
87 citing papers in PubMed, 249 citations in OpenAlex.
- DNA Methylation Shapes Seed-Borne Microbiome and Proteome Responses During Early Maize-Beneficial Bacteria Interactions.Plant, cell & environment · 2026Article
- Light-Activatable MBD-Readers of 5-Methylcytosine Reveal Domain-Dependent Chromatin Association Kinetics In Vivo.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Optochemical Control of TET Dioxygenases Enables Kinetic Insights into the Domain-Dependent Interplay of TET1 and MBD1 while Oxidizing and Reading 5-Methylcytosine.ACS chemical biology · 2022Article
- Role of DNMTs in the Brain.Advances in experimental medicine and biology · 2022Review
- The fibronectin type-III (FNIII) domain of ATF7IP contributes to efficient transcriptional silencing mediated by the SETDB1 complex.Epigenetics & chromatin · 2020Article
- MBD1 Contributes to the Genesis of Acute Pain and Neuropathic Pain by Epigenetic Silencing ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Epigenetic regulation of MAGE family in human cancer progression-DNA methylation, histone modification, and non-coding RNAs.Clinical epigenetics · 2018Review
- Readers of DNA methylation, the MBD family as potential therapeutic targets.Pharmacology & therapeutics · 2018Review
- MAGE-A11 is activated through TFCP2/ZEB1 binding sites de-methylation as well as histone modification and facilitates ESCC tumor growth.Oncotarget · 2018Article
- Comprehensive identification of proteins binding to RNA G-quadruplex motifs in the 5' UTR of tumor-associated mRNAs.Biochimie · 2018Article
- DNA Methylation and Adult Neurogenesis.Brain plasticity (Amsterdam, Netherlands) · 2017Review
- Article
- Methyl-CpG-binding protein MBD2 plays a key role in maintenance and spread of DNA methylation at CpG islands and shores in cancer.Oncogene · 2017Article
- Methyl-CpG-Binding Protein MBD1 Regulates Neuronal Lineage Commitment through Maintaining Adult Neural Stem Cell Identity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Tagging methyl-CpG-binding domain proteins reveals different spatiotemporal expression and supports distinct functions.Epigenomics · 2016Article
- Modifiers and Readers of DNA Modifications and Their Impact on Genome Structure, Expression, and Stability in Disease.Frontiers in genetics · 2016Review
- Analysis of the SUMO2 Proteome during HSV-1 Infection.PLoS pathogens · 2015Article
- An epigenetic regulator: methyl-CpG-binding domain protein 1 (MBD1).International journal of molecular sciences · 2015Review
- Targeting polycomb to pericentric heterochromatin in embryonic stem cells reveals a role for H2AK119u1 in PRC2 recruitment.Cell reports · 2014Article
- Transcriptional repressor domain of MBD1 is intrinsically disordered and interacts with its binding partners in a selective manner.Scientific reports · 2014Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
MBD1 belongs to a family of mammalian proteins that share a methyl-CpG binding domain. Previous work has shown that MBD1 binds to methylated sites in vivo and in vitro and can repress transcription from methylated templates in transcription extracts and in cultured cells. In the present study we established by several experimental criteria that, contrary to a previous report, MBD1 is not a component of the MeCP1 repressor complex. We identified a powerful transcriptional repression domain (TRD) at the C terminus of MBD1 that can actively repress transcription at a distance. Methylation-dependent repression in vivo depends on the presence of both the TRD and the methyl-CpG binding domain. The mechanism is likely to involve deacetylation, since the deacetylase inhibitor trichostatin A can overcome MBD1-mediated repression. Accordingly, we found that endogenous MBD1 is particularly concentrated at sites of centromeric heterochromatin, where acetylated histone H4 is deficient. Unlike MBD2 and MeCP2, MBD1 is not depleted by antibodies to the histone deacetylase HDAC1. Thus, the deacetylase-dependent pathway by which MBD1 actively silences methylated genes is likely to be different from that utilized by the methylation-dependent repressors MeCP1 and MeCP2.
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.