ArticleScientific reports2014
Transcriptional repressor domain of MBD1 is intrinsically disordered and interacts with its binding partners in a selective manner.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Gene regulatory mechanisms downstream of DNA methylation.Nature reviews. Genetics · 2026Review
- Light-Activatable MBD-Readers of 5-Methylcytosine Reveal Domain-Dependent Chromatin Association Kinetics In Vivo.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- MBD1 protects replication fork stability by recruiting PARP1 and controlling transcription-replication conflicts.Cancer gene therapy · 2024Article
- Genome-wide identification of MBD gene family members in Eleutherococcus senticosus with their expression motifs under drought stress and DNA demethylation.BMC genomics · 2023Article
- Article
- 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
- Roles, Characteristics, and Analysis of Intrinsically Disordered Proteins: A Minireview.Life (Basel, Switzerland) · 2020Review
- High Resolution Imaging of DNA Methylation Dynamics using a Zebrafish Reporter.Scientific reports · 2017Article
- 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 · 2017Article
- An intrinsically disordered region of methyl-CpG binding domain protein 2 (MBD2) recruits the histone deacetylase core of the NuRD complex.Nucleic acids research · 2015Article
- An epigenetic regulator: methyl-CpG-binding domain protein 1 (MBD1).International journal of molecular sciences · 2015Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methylation of DNA CpG sites is a major mechanism of epigenetic gene silencing and plays important roles in cell division, development and carcinogenesis. One of its regulators is the 64-residue C-terminal Transcriptional Repressor Domain (the TRD) of MBD1, which recruits several repressor proteins such as MCAF1, HDAC3 and MPG that are essential for the gene silencing. Using NMR spectroscopy, we have characterized the solution structure of the C-terminus of MBD1 (MBD1-c, residues D507 to Q605), which included the TRD (A529 to P592). Surprisingly, the MBD1-c is intrinsically disordered. Despite its lack of a tertiary folding, MBD1-c could still bind to different partner proteins in a selective manner. MPG and MCAF1Δ8 showed binding to both the N-terminal and C-terminal residues of MBD1-c but HDAC3 preferably bound to the C-terminal region. This study reveals how MBD1-c discriminates different binding partners, and thus, expands our understanding of the mechanisms of gene regulation by MBD1.
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