ArticlePloS one2013
Structural and functional analysis of the DEAF-1 and BS69 MYND domains.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- The chromatin reader ZMYND8 recruits the NuRD component GATAD2A through its MYND domain to regulate MAPT213 long noncoding RNA transcription.The Journal of biological chemistry · 2026Article
- ZMYND11 p.Arg600Trp variant associated with a distinctive neurodevelopmental phenotype.Human genome variation · 2026Article
- ZMYND11 Restrains KMT2A to Enable a Neuronal Developmental Program.bioRxiv : the preprint server for biology · 2025Article
- Conserved transcription factors coordinate synaptic gene expression through repression.bioRxiv : the preprint server for biology · 2025Article
- Zinc finger myeloid Nervy DEAF-1 type (ZMYND) domain containing proteins exert molecular interactions to implicate in carcinogenesis.Discover oncology · 2022Review
- Article
- De novo and biallelic DEAF1 variants cause a phenotypic spectrum.Genetics in medicine : official journal of the American College of Medical Genetics · 2019Article
- Is MYND Domain-Mediated Assembly of SMYD3 Complexes Involved in Calcium Dependent Signaling?Frontiers in molecular biosciences · 2019Article
- The Transcriptional Repressor BS69 is a Conserved Target of the E1A Proteins from Several Human Adenovirus Species.Viruses · 2018Article
- BS69/ZMYND11 C-Terminal Domains Bind and Inhibit EBNA2.PLoS pathogens · 2016Article
- Structure and function of SET and MYND domain-containing proteins.International journal of molecular sciences · 2015Review
- Article
- Refining analyses of copy number variation identifies specific genes associated with developmental delay.Nature genetics · 2014Article
- Mutations affecting the SAND domain of DEAF1 cause intellectual disability with severe speech impairment and behavioral problems.American journal of human genetics · 2014Article
- Article
- Zinc finger structure determination by NMR: Why zinc fingers can be a handful.Progress in nuclear magnetic resonance spectroscopyReview
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DEAF-1 is an important transcriptional regulator that is required for embryonic development and is linked to clinical depression and suicidal behavior in humans. It comprises various structural domains, including a SAND domain that mediates DNA binding and a MYND domain, a cysteine-rich module organized in a Cys(4)-Cys(2)-His-Cys (C4-C2HC) tandem zinc binding motif. DEAF-1 transcription regulation activity is mediated through interactions with cofactors such as NCoR and SMRT. Despite the important biological role of the DEAF-1 protein, little is known regarding the structure and binding properties of its MYND domain.Here, we report the solution structure, dynamics and ligand binding of the human DEAF-1 MYND domain encompassing residues 501-544 determined by NMR spectroscopy. The structure adopts a ββα fold that exhibits tandem zinc-binding sites with a cross-brace topology, similar to the MYND domains in AML1/ETO and other proteins. We show that the DEAF-1 MYND domain binds to peptides derived from SMRT and NCoR corepressors. The binding surface mapped by NMR titrations is similar to the one previously reported for AML1/ETO. The ligand binding and molecular functions of the related BS69 MYND domain were studied based on a homology model and mutational analysis. Interestingly, the interaction between BS69 and its binding partners (viral and cellular proteins) seems to require distinct charged residues flanking the predicted MYND domain fold, suggesting a different binding mode. Our findings demonstrate that the MYND domain is a conserved zinc binding fold that plays important roles in transcriptional regulation by mediating distinct molecular interactions with viral and cellular proteins.
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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.