Affinage

ZMYND11

Zinc finger MYND domain-containing protein 11 · UniProt Q15326

Length
602 aa
Mass
71.0 kDa
Annotated
2026-04-28
59 papers in source corpus 28 papers cited in narrative 29 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ZMYND11 (BS69) is a multidomain chromatin reader and transcriptional co-repressor that couples histone variant–specific recognition to regulation of transcription elongation, RNA splicing, and signaling. Its tandem bromo-PWWP domains form a composite pocket that specifically recognizes H3.3K36me3 via the H3.3-unique Ser31 residue, directing ZMYND11 to active gene bodies where it modulates RNA polymerase II elongation and promotes intron retention by antagonizing the spliceosome component EFTUD2 (PMID:24590075, PMID:25263594). The C-terminal MYND domain, which folds as a ββα zinc-binding module and functions as a homodimer via the coiled-coil region, serves as a protein–protein interaction hub that engages PXLXP-motif partners (E1A, EBNA2, MGA), co-repressor N-CoR, TRAF6/TRAF3 to modulate NF-κB and JNK signaling, the histone methyltransferase KMT2A whose inhibition it mediates, and arginine-methylated nonhistone substrates such as HNRNPA1 to control stress granule formation (PMID:11733528, PMID:26845565, PMID:16382137, PMID:39341825, PMID:41279818). ZMYND11 suppresses cellular senescence through the p53–p21Cip1 axis, regulates brain-specific RBFOX2-dependent splicing programs essential for neurogenesis and dendritic morphogenesis, and its loss in neurons causes upregulation of non-neuronal genes and behavioral abnormalities (PMID:17721438, PMID:41068108, PMID:40281637).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1995 High

    The initial identification of BS69/ZMYND11 as a nuclear phosphoprotein that binds adenovirus E1A CR3 and inhibits E1A-mediated transactivation established it as a transcriptional repressor.

    Evidence Co-IP from adenovirus-transformed 293 cells plus transactivation reporter assays and yeast two-hybrid

    PMID:7621829

    Open questions at the time
    • Endogenous target genes unknown
    • Mechanism of repression unresolved
    • Physiological relevance beyond viral context unclear
  2. 1998 Medium

    Discovery of the cytoplasmic isoform BRAM1, which binds BMP receptor IA, revealed that alternative splicing generates isoforms with distinct subcellular localization and potentially different signaling functions.

    Evidence Yeast two-hybrid with Co-IP in mammalian cells; subcellular fractionation and immunofluorescence

    PMID:9663660

    Open questions at the time
    • Functional consequence of BRAM1–BMPR-IA interaction on BMP signaling not demonstrated
    • Tissue-specific expression of isoforms not characterized
  3. 2001 High

    Mapping the MYND domain as the binding interface for a conserved PXLXP motif shared by viral (E1A, EBNA2) and cellular (MGA) partners established a general recognition mechanism and revealed that viral oncoproteins hijack a host protein–protein interaction surface.

    Evidence GST pulldown, yeast two-hybrid, Co-IP, and PXLXP mutagenesis with competition assays; interaction with N-CoR via MYND domain and repression of c-Myb

    PMID:10734313 PMID:11244510 PMID:11733528

    Open questions at the time
    • Structural basis of MYND–PXLXP recognition not yet determined
    • Full complement of cellular PXLXP partners unknown
  4. 2006 High

    Demonstration that BS69 bridges EBV LMP1 to TRAF6 to specifically activate JNK signaling, and association with chromatin-remodeling complexes and E2F6, broadened its role from simple repressor to a signal-transduction adaptor and chromatin organizer.

    Evidence Reciprocal Co-IP, siRNA knockdown with JNK kinase assay and chimeric rescue; endogenous IP–mass spectrometry and chromatin fractionation

    PMID:16382137 PMID:16565076

    Open questions at the time
    • Structural mechanism of TRAF6 bridging unclear
    • Whether chromatin-associated complexes are functionally distinct from signaling complexes not tested
  5. 2007 High

    Linking BS69 to cellular senescence through the p53–p21Cip1 pathway provided the first endogenous physiological function, showing that BS69 forms complexes with p53 and p400 on the p21 promoter to suppress premature senescence.

    Evidence siRNA and double-knockdown epistasis, ChIP at p21 promoter, Co-IP with p53 and p400, senescence assays in primary fibroblasts

    PMID:17721438

    Open questions at the time
    • Whether BS69 directly represses p21 transcription or acts through p400 remodeling not resolved
    • Relevance to in vivo aging or tumor suppression not tested
  6. 2009 Medium

    Multiple studies established that BS69 modulates NF-κB signaling (both LMP1-induced and TICAM-1/dsRNA-induced pathways) and undergoes SUMO modification by PIAS1, revealing post-translational regulation and context-dependent pro- or anti-inflammatory roles.

    Evidence Co-IP, NF-κB and IFN-β reporter assays, siRNA, confocal imaging of nuclear-cytoplasmic translocation; in vivo SUMOylation assay with domain mutagenesis

    PMID:19379743 PMID:19766626 PMID:19795416

    Open questions at the time
    • How SUMOylation affects BS69 transcriptional or signaling activity not determined
    • Opposing effects on NF-κB in different contexts not mechanistically reconciled
  7. 2014 High

    Crystal structure and ChIP-seq demonstrated that ZMYND11 is a histone-variant-specific reader recognizing H3.3K36me3 through a composite bromo-PWWP pocket encapsulating H3.3 Ser31, and that this recognition directs it to gene bodies to modulate Pol II elongation and RNA splicing (intron retention via EFTUD2 antagonism), establishing its core chromatin-based mechanism.

    Evidence Crystal structure, ChIP-seq, in vitro binding assays, RNA-seq, Co-IP with U5 snRNP/EFTUD2, genetic epistasis

    PMID:24590075 PMID:25263594

    Open questions at the time
    • How H3.3K36me3 binding is mechanistically linked to Pol II pausing/elongation not fully elucidated
    • Genome-wide determinants of which genes are repressed vs. spliced unclear
  8. 2016 High

    Crystal structure of the CC-MYND homodimer bound to EBNA2 PXLXP motifs revealed that coiled-coil-mediated dimerization brings two MYND domains into proximity for synergistic bivalent binding, providing a structural explanation for high-affinity target recognition.

    Evidence Crystal structure of CC-MYND/EBNA2 complex, ITC binding quantification, mutagenesis, reporter assays

    PMID:26845565

    Open questions at the time
    • Whether dimerization similarly enhances binding to all cellular PXLXP partners untested
    • Regulation of dimer formation not addressed
  9. 2021 High

    Studies of the ZMYND11-MBTD1 leukemia fusion showed that the ZMYND11 PWWP domain's H3K36me3 reading function is co-opted to mislocalize the NuA4/TIP60 acetyltransferase complex to gene bodies, driving aberrant chromatin acetylation and pro-leukemic gene expression.

    Evidence ChIP-seq, ATAC-seq, systematic mutagenesis, Co-IP, in vivo leukemia model; biochemical co-purification confirming stable incorporation into endogenous NuA4/TIP60

    PMID:33594072 PMID:35705031

    Open questions at the time
    • Whether wild-type ZMYND11 normally opposes NuA4/TIP60 at gene bodies not tested
    • Patient-relevant therapeutic vulnerabilities not fully defined
  10. 2024 Medium

    Discovery that the MYND domain reads arginine-methylated HNRNPA1 (R194me, deposited by PRMT5) extended ZMYND11 from a histone reader to a nonhistone methylation reader, linking it to stress granule suppression and PKM splicing regulation in tumor suppression.

    Evidence Co-IP, domain mutagenesis, subcellular fractionation, in vitro and in vivo tumor assays, pharmacological PRMT5 inhibition

    PMID:39341825

    Open questions at the time
    • Breadth of nonhistone methylated substrates recognized by MYND domain unknown
    • In vivo relevance of stress granule regulation not confirmed in animal models
  11. 2025 Medium

    ZMYND11 was shown to inhibit the histone methyltransferase KMT2A, regulate RBFOX2-dependent brain-specific splicing, and control neurogenesis via EPHA2-PI3K signaling; neuronal loss causes dendritic defects and behavioral abnormalities linked to neurodevelopmental disorder (ZRSID).

    Evidence Co-IP with disease-associated mutagenesis, degron-tagged and conditional knockout mouse models, RNA-seq, ChIP, pharmacological KMT2A inhibition with revumenib, human cortical organoid differentiation

    PMID:40281637 PMID:41068108 PMID:41279818

    Open questions at the time
    • Precise molecular mechanism of KMT2A inhibition not structurally resolved
    • Whether splicing and KMT2A-regulation are independent or linked pathways unclear
    • PMID:41279818 is a preprint awaiting peer review
  12. 2026 High

    Comprehensive structural characterization revealed that PHD domain intermolecular zinc fingers and CC-MYND redox-driven disulfide bonds regulate oligomeric state and substrate binding, with the WH domain contributing to nucleic acid binding and PHD/CC-MYND domains interacting with the nucleic acid repair protein ALKBH6.

    Evidence Multiple crystal structures, ITC, mutagenesis, Co-IP

    PMID:41591843

    Open questions at the time
    • Functional significance of ALKBH6 interaction not established in cells
    • How redox sensing regulates ZMYND11 function in vivo unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • Major unresolved questions include how ZMYND11's chromatin-reading, splicing-regulatory, signaling-adaptor, and nonhistone-reader functions are coordinated in different cell types, the full repertoire of arginine-methylated substrates, and the precise molecular mechanism by which H3.3K36me3 binding is transduced into Pol II elongation control.
  • Integration of chromatin, splicing, and signaling functions not mechanistically unified
  • Structural basis of Pol II elongation modulation unknown
  • Complete interactome of arginine-methylated nonhistone substrates not defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 6 GO:0042393 histone binding 4 GO:0060090 molecular adaptor activity 2 GO:0098772 molecular function regulator activity 2 GO:0003677 DNA binding 1
Localization
GO:0005634 nucleus 4 GO:0005829 cytosol 2 GO:0005694 chromosome 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-4839726 Chromatin organization 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-1266738 Developmental Biology 2 R-HSA-8953854 Metabolism of RNA 2
Partners
EBNA2EFTUD2HNRNPA1KMT2APIAS1TRAF3TRAF6USP53
Complex memberships
NuA4/TIP60 (via ZMYND11-MBTD1 fusion)

Evidence

Reading pass · 29 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2014 ZMYND11 specifically recognizes H3K36me3 on histone variant H3.3 (H3.3K36me3) through its tandem bromo-PWWP domains; the PWWP domain provides an aromatic cage for trimethyl-lysine binding, while the H3.3-specific Ser31 residue is encapsulated in a composite pocket formed by the bromo-PWWP domains together. Structural studies (crystal structure), chromatin immunoprecipitation followed by sequencing (ChIP-seq), in vitro binding assays Nature High 24590075
2014 ZMYND11 functions as an unconventional transcriptional co-repressor by modulating RNA polymerase II at the elongation stage; genome-wide occupancy requires pre-deposition of H3.3K36me3 in gene bodies. ChIP-seq, RNA polymerase II elongation assays, loss-of-function experiments in cancer cells Nature High 24590075
2014 ZMYND11 (BS69) associates with RNA splicing regulators including U5 snRNP components (e.g., EFTUD2) and promotes intron retention by antagonizing EFTUD2 through physical interaction; this regulation also depends on binding to H3K36me3-decorated chromatin. Co-immunoprecipitation, RNA sequencing, biochemical and genetic epistasis experiments Molecular cell High 25263594
1995 BS69 (ZMYND11) was identified as a nuclear phosphoprotein that interacts specifically with the conserved region 3 (CR3) of the adenovirus 5 289R E1A protein and inhibits E1A-mediated transcriptional transactivation; interaction was confirmed by co-immunoprecipitation in adenovirus-transformed 293 cells. Co-immunoprecipitation, transactivation reporter assays, yeast two-hybrid The EMBO journal High 7621829
2000 BS69 mediates transcriptional repression at least in part through interaction with the co-repressor N-CoR via its MYND domain; expression of E1A inhibits repression mediated by BS69. Co-immunoprecipitation, transcriptional reporter assays, domain deletion analysis Oncogene Medium 10734313
2001 The C-terminal MYND domain of BS69 binds to viral (E1A, EBNA2) and cellular (MGA) proteins through a conserved PXLXP motif; viral proteins compete with MGA for BS69 MYND binding in a PXLXP-dependent manner. GST pulldown, yeast two-hybrid, co-immunoprecipitation, mutagenesis The Journal of biological chemistry High 11733528
2001 BS69 interacts with the carboxyl terminus of c-Myb via its MYND domain and inhibits c-Myb transcriptional activity in a dose-dependent manner; direct interaction was demonstrated in vitro, and 289R E1A can relieve BS69-mediated repression of c-Myb. Yeast two-hybrid, in vitro GST pulldown, transcriptional reporter assays Oncogene Medium 11244510
1998 BRAM1, an alternatively spliced isoform of BS69/ZMYND11, is localized to the cytoplasm (unlike nuclear BS69) and specifically binds to BMPR-IA (BMP type IA receptor) via its C-terminal half. Yeast two-hybrid, co-immunoprecipitation in mammalian cells, subcellular localization by cell fractionation/immunofluorescence Genes to cells Medium 9663660
2006 BS69's MYND domain acts as a specific adaptor bridging EBV LMP1 and TRAF6 to activate the JNK pathway; the MYND domain binds LMP1 C-terminus while a separate region binds TRAF6; LMP1 promotes the BS69-TRAF6 complex, and knockdown of BS69 specifically inhibits LMP1-induced JNK activation but not TNF-alpha-induced JNK activation. Co-immunoprecipitation, siRNA knockdown, JNK kinase assays, chimeric protein rescue Molecular and cellular biology High 16382137
2006 BS69 associates with chromatin remodeling factors including ATP-dependent helicases, histone deacetylases, histone methyltransferases, and the transcription factor E2F6; BS69 is nuclear and associates with chromatin and mitotic chromosomes. Endogenous protein immunoprecipitation, mass spectrometry, chromatin fractionation, immunofluorescence The Journal of biological chemistry Medium 16565076
2007 BS69 is involved in cellular senescence through the p53-p21Cip1 pathway; knockdown of BS69 in primary fibroblasts elevates p21Cip1 and induces premature senescence that is bypassed by knockdown of p53 or p21Cip1 (but not p16 or Rb); BS69 forms complexes with p53 and p400 and associates with the p21Cip1 promoter via p53. siRNA knockdown, double knockdown epistasis, chromatin immunoprecipitation, co-immunoprecipitation, senescence assays EMBO reports High 17721438
2009 BS69 undergoes SUMO modification; it interacts with SUMO E3 ligase PIAS1 and SUMO E2 enzyme Ubc9 through distinct domains, and PIAS1 significantly increases BS69 SUMOylation; the PHD domain is required for proper localization, sumoylation, and function of BS69. Co-immunoprecipitation, in vivo SUMOylation assay, domain mutant analysis, immunofluorescence Experimental cell research Medium 19766626
2009 BS69 negatively regulates LMP1-mediated NF-κB activation by decreasing complex formation between LMP1 and TRADD; manipulation of BS69 expression modulates IκBα degradation and IL-6 production. siRNA knockdown, overexpression, co-immunoprecipitation, NF-κB reporter assay FEBS letters Medium 19379743
2009 BS69 translocates from the nucleus to the cytoplasm upon dsRNA stimulation or TICAM-1 overexpression, where it is incorporated into the TICAM-1 signalosome complex and acts as a positive regulator of NF-κB and IRF-3 activation and IFN-β induction. Yeast two-hybrid, co-immunoprecipitation, confocal microscopy, siRNA knockdown, reporter assays European journal of immunology Medium 19795416
2010 BS69 directly interacts with the LMP1/CTAR1 domain and with TRAF3, and BS69-mediated suppression of LMP1/CTAR1-induced NF-κB activation requires TRAF3. Co-immunoprecipitation, siRNA knockdown, NF-κB reporter assays FEBS letters Medium 20138174
2013 The BS69 MYND domain folds as a ββα zinc binding domain (C4-C2HC topology); mutational analysis of charged residues flanking the MYND fold reveals they are required for binding to viral (E1A, EBNA2) and cellular partners, suggesting a distinct binding mode from related MYND domains. NMR structure (DEAF-1 MYND), homology modeling, mutagenesis, NMR titration binding assays PloS one Medium 23372760
2016 The BS69/ZMYND11 coiled-coil domain self-associates to bring two MYND domains into proximity, enhancing binding to EBNA2 PXLXP motifs; the CC-MYND homodimer synergistically binds the two PXLXP motifs in EBNA2 CR7 and CR8; EBNA2 also down-regulates BS69 expression in EBV-infected B cells. Crystal structure of CC-MYND/EBNA2 complex, ITC binding analysis, mutagenesis, reporter assays, ectopic expression experiments PLoS pathogens High 26845565
2017 ZMYND11 specifically interacts with ETS2 (but not ETS1) through the ETS2 N-terminus and attenuates ETS2 transcriptional activation, causing ETS2 to repress rather than activate a cell migration gene expression program; this interaction underlies the context-dependent oncogenic vs. tumor-suppressive function of ETS2. Co-immunoprecipitation, ETS1/ETS2 cistrome comparison (ChIP-seq), deletion mapping, reporter assays Nucleic acids research Medium 28119415
2019 Type 2 EBV EBNA2 contains a third PXLXP motif that allows binding of an additional BS69 CC-MYND dimer; SAXS shows three BS69CC-MYND dimers bind two molecules of type 2 EBNA2 TAD; mutation of the third BS69-binding motif in type 2 EBNA2 improved B-cell growth and transcriptional activation. Pull-down assays, small-angle X-ray scattering (SAXS), mutagenesis, transcriptional and B-cell growth assays PLoS pathogens High 31283782
2014 MAGE-C2/HCA587 interacts with BS69 and promotes its ubiquitination and proteasomal degradation; knockdown of HCA587 increases BS69 protein levels, and overexpression of HCA587 enhances LMP1-induced NF-κB activation consistent with reduced BS69 levels. Co-immunoprecipitation, mass spectrometry, GST pulldown, ubiquitination assay, proteasome inhibitor treatment Biochemical and biophysical research communications Medium 24866244
2005 BS69 inhibits ubiquitination of adenovirus E1A protein through its MYND domain; BS69 binding to E1A protects E1A from proteasomal degradation; MYND domain mutants that cannot bind E1A fail to inhibit E1A ubiquitination. In vivo ubiquitination assay, proteasome inhibitor experiments, MYND domain mutagenesis, co-immunoprecipitation Biochemical and biophysical research communications Medium 16300738
2021 The ZMYND11-MBTD1 fusion oncoprotein recruits the NuA4/TIP60 histone acetyltransferase complex to cis-regulatory elements of pro-leukemic genes via the ZMYND11 PWWP domain's H3K36me3 binding, sustaining active chromatin enriched in histone acetylation; both TIP60 interaction and the PWWP H3K36me3-binding are required for oncogenesis. ChIP-seq, ATAC-seq, systematic mutagenesis, co-immunoprecipitation, in vivo leukemia model, gene expression profiling Nature communications High 33594072
2022 ZMYND11-MBTD1 is stably incorporated into the endogenous NuA4/TIP60 complex, mislocalizing it to the bodies of genes normally bound by ZMYND11; this leads to increased chromatin acetylation and altered gene transcription including on MYC, and alternative splicing changes. Biochemical co-purification/Co-IP, ChIP-seq, RNA-seq, comparison to individual fusion partners Cell reports High 35705031
2024 ZMYND11 exhibits a non-canonical function as a nonhistone methylation reader: its MYND domain recognizes arginine-194-methylated HNRNPA1, retaining HNRNPA1 in the nucleus and preventing stress granule formation in the cytoplasm; ZMYND11 also counteracts HNRNPA1-driven increases in PKM2/PKM1 ratio; PRMT5 inhibition disrupts the ZMYND11-HNRNPA1 interaction. Co-immunoprecipitation, domain mutagenesis, subcellular fractionation, in vitro and in vivo tumor assays, pharmacological PRMT5 inhibition Signal transduction and targeted therapy Medium 39341825
2024 USP53 deubiquitinase interacts with ZMYND11 via co-immunoprecipitation and catalyzes its deubiquitination and stabilization; the USP53 Cys-box domain (aa 33-50) is required for enzyme activity but not for ZMYND11 binding; loss of USP53 reduces ZMYND11 protein levels and promotes breast cancer cell growth. Co-immunoprecipitation, deubiquitination assay, loss-of-function and rescue experiments Biological procedures online Medium 39044157
2025 ZMYND11 interacts with and inhibits the histone methyltransferase KMT2A (MLL1); a ZRSID-associated ZMYND11 point mutation abrogates this interaction; neuronal deletion of ZMYND11 causes upregulation of non-neuronal gene programs and reduced dendritic branching, effects attenuated by KMT2A inhibition with revumenib. Co-immunoprecipitation, point mutagenesis, degron-tagged mouse model, RNA-seq, dendritic morphology assay, pharmacological KMT2A inhibition bioRxivpreprint Medium 41279818
2025 ZMYND11 regulates a brain-specific RNA isoform switch involving the splicing regulator RBFOX2; ZMYND11-deficient cortical neural stem cells upregulate inappropriate developmental pathways impairing neurogenesis, and similar splicing dysregulation is seen with other chromatin-related ASD risk genes. Human pluripotent stem cell differentiation model, RNA-seq, loss-of-function Nature communications Medium 41068108
2026 Crystal structures of ZMYND11 WH, PHD, and CC-MYND domains reveal intermolecular zinc fingers (PHD domain) and redox-driven intermolecular disulfide bonds (CC-MYND domain) that regulate oligomeric state and substrate binding; the Bromo-PWWP domains cooperate with WH to bind nucleic acids and with PHD to bind histones; PHD and CC-MYND domains also interact with nucleic acid repair protein ALKBH6. Crystal structure determination, ITC, mutagenesis, co-immunoprecipitation Nucleic acids research High 41591843
2025 In mouse neurons, ZMYND11 deficiency leads to upregulation of non-neuronal gene programs, reduced dendritic branching and spine density, and hyperactivity/abnormal motor behavior; Zmynd11 deficiency in embryos impairs neurogenesis by decreasing Epha2 expression, increasing H3K36me3 on the Epha2 promoter, and disrupting PI3K signaling; restoration of PI3K via Epha2 rescues neurogenesis defects. Conditional neuronal knockout mouse, degron model, ChIP for H3K36me3, RNA Pol II ChIP, Epha2 rescue experiments, behavioral assays Cell & bioscience Medium 40281637

Source papers

Stage 0 corpus · 59 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 ZMYND11 links histone H3.3K36me3 to transcription elongation and tumour suppression. Nature 262 24590075
2014 BS69/ZMYND11 reads and connects histone H3.3 lysine 36 trimethylation-decorated chromatin to regulated pre-mRNA processing. Molecular cell 186 25263594
1995 BS69, a novel adenovirus E1A-associated protein that inhibits E1A transactivation. The EMBO journal 80 7621829
2001 The conserved Mynd domain of BS69 binds cellular and oncoviral proteins through a common PXLXP motif. The Journal of biological chemistry 77 11733528
2000 The adenovirus E1A binding protein BS69 is a corepressor of transcription through recruitment of N-CoR. Oncogene 70 10734313
2001 BS69, an adenovirus E1A-associated protein, inhibits the transcriptional activity of c-Myb. Oncogene 53 11244510
1998 BRAM1, a BMP receptor-associated molecule involved in BMP signalling. Genes to cells : devoted to molecular & cellular mechanisms 44 9663660
2006 BS69, a specific adaptor in the latent membrane protein 1-mediated c-Jun N-terminal kinase pathway. Molecular and cellular biology 39 16382137
2021 ZMYND11-MBTD1 induces leukemogenesis through hijacking NuA4/TIP60 acetyltransferase complex and a PWWP-mediated chromatin association mechanism. Nature communications 36 33594072
2006 New insights into BS69 functions. The Journal of biological chemistry 28 16565076
2014 A de novo mutation in ZMYND11, a candidate gene for 10p15.3 deletion syndrome, is associated with syndromic intellectual disability. European journal of medical genetics 27 25281490
2005 Binding of EMSY to HP1beta: implications for recruitment of HP1beta and BS69. EMBO reports 27 15947784
2017 Interaction with ZMYND11 mediates opposing roles of Ras-responsive transcription factors ETS1 and ETS2. Nucleic acids research 25 28119415
2017 Phenotype comparison confirms ZMYND11 as a critical gene for 10p15.3 microdeletion syndrome. Journal of applied genetics 24 28933030
2017 Downregulation of ZMYND11 induced by miR-196a-5p promotes the progression and growth of GBM. Biochemical and biophysical research communications 24 29066350
2016 A de novo missense mutation in ZMYND11 is associated with global developmental delay, seizures, and hypotonia. Cold Spring Harbor molecular case studies 23 27626064
2020 ZMYND11-related syndromic intellectual disability: 16 patients delineating and expanding the phenotypic spectrum. Human mutation 22 32097528
2016 BS69/ZMYND11 C-Terminal Domains Bind and Inhibit EBNA2. PLoS pathogens 22 26845565
2009 BS69 negatively regulates the canonical NF-kappaB activation induced by Epstein-Barr virus-derived LMP1. FEBS letters 22 19379743
2013 Structural and functional analysis of the DEAF-1 and BS69 MYND domains. PloS one 21 23372760
2019 Increased association between Epstein-Barr virus EBNA2 from type 2 strains and the transcriptional repressor BS69 restricts EBNA2 activity. PLoS pathogens 20 31283782
2016 Chicken gga-miR-19a Targets ZMYND11 and Plays an Important Role in Host Defense against Mycoplasma gallisepticum (HS Strain) Infection. Frontiers in cellular and infection microbiology 20 27683641
2020 Hsa_circ_0008225 inhibits tumorigenesis of glioma via sponging miR-890 and promoting ZMYND11 expression. Journal of pharmacological sciences 19 32192854
2015 Recurrent translocation t(10;17)(p15;q21) in minimally differentiated acute myeloid leukemia results in ZMYND11/MBTD1 fusion. Genes, chromosomes & cancer 19 26608508
2021 MicroRNA-196a promotes renal cancer cell migration and invasion by targeting BRAM1 to regulate SMAD and MAPK signaling pathways. International journal of biological sciences 17 34803496
2019 Gga-miR-19b-3p Inhibits Newcastle Disease Virus Replication by Suppressing Inflammatory Response via Targeting RNF11 and ZMYND11. Frontiers in microbiology 16 31507581
2002 Negative regulation of Epstein-Barr virus latent membrane protein 1-mediated functions by the bone morphogenetic protein receptor IA-binding protein, BRAM1. The Journal of biological chemistry 15 12181323
2024 Epigenetic reader ZMYND11 noncanonical function restricts HNRNPA1-mediated stress granule formation and oncogenic activity. Signal transduction and targeted therapy 14 39341825
2010 BS69 cooperates with TRAF3 in the regulation of Epstein-Barr virus-derived LMP1/CTAR1-induced NF-kappaB activation. FEBS letters 14 20138174
2007 BS69, a corepressor interacting with ZHX1, is a bifunctional transcription factor. Frontiers in bioscience : a journal and virtual library 14 17127430
2007 BS69 is involved in cellular senescence through the p53-p21Cip1 pathway. EMBO reports 13 17721438
2021 ZMYND11 variants are a novel cause of centrotemporal and generalised epilepsies with neurodevelopmental disorder. Clinical genetics 12 34216016
2009 BS69 undergoes SUMO modification and plays an inhibitory role in muscle and neuronal differentiation. Experimental cell research 12 19766626
2014 Cancer-testis antigen HCA587/MAGE-C2 interacts with BS69 and promotes its degradation in the ubiquitin-proteasome pathway. Biochemical and biophysical research communications 11 24866244
2022 Oncogenic ZMYND11-MBTD1 fusion protein anchors the NuA4/TIP60 histone acetyltransferase complex to the coding region of active genes. Cell reports 10 35705031
2005 Ubiquitin-dependent degradation of adenovirus E1A protein is inhibited by BS69. Biochemical and biophysical research communications 10 16300738
2024 USP53 Affects the Proliferation and Apoptosis of Breast Cancer Cells by Regulating the Ubiquitination Level of ZMYND11. Biological procedures online 8 39044157
2010 Analysis of copy number variations of BS69 in multiple types of hematological malignancies. Annals of hematology 8 20425112
2009 Oligomerized TICAM-1 (TRIF) in the cytoplasm recruits nuclear BS69 to enhance NF-kappaB activation and type I IFN induction. European journal of immunology 8 19795416
2018 Mga Modulates Bmpr1a Activity by Antagonizing Bs69 in Zebrafish. Frontiers in cell and developmental biology 7 30324105
2018 The Transcriptional Repressor BS69 is a Conserved Target of the E1A Proteins from Several Human Adenovirus Species. Viruses 7 30469473
2021 Intragenic Deletion of the ZMYND11 Gene in 10p15.3 is Associated with Developmental Delay Phenotype: A Case Report. Cytogenetic and genome research 6 34818214
2020 MicroRNA-196b promotes cell growth and metastasis of ovarian cancer by targeting ZMYND11. Minerva medica 5 32512976
2019 Regulation of BS69 Expression in Cancers. Anticancer research 5 31262855
2006 Molecular cloning, expression and characterization of the zebrafish bram1 gene, a BMP receptor-associated molecule. Journal of biomedical science 5 16456708
2024 Further Delineation of Clinical Phenotype of ZMYND11 Variants in Patients with Neurodevelopmental Dysmorphic Syndrome. Genes 4 38397245
2010 The MYND domain-containing protein BRAM1 inhibits lymphotoxin beta receptor-mediated signaling through affecting receptor oligomerization. Cellular signalling 4 20732415
2025 ZMYND11 functions in bimodal regulation of latent genes and brain-like splicing to safeguard corticogenesis. Nature communications 3 41068108
2024 Probing the biological consequences of a previously undescribed de novo mutation of ZMYND11 in a schizophrenia patient by CRISPR genome editing and induced pluripotent stem cell based in vitro disease-modeling. Schizophrenia research 3 38290943
2023 Transgenic mice overexpressing mutant TDP-43 show aberrant splicing of neurological disorders-associated gene Zmynd11 prior to onset of motor symptoms. microPublication biology 3 37008727
2024 Acute myeloid leukemia with a ZMYND11::MBTD1 fusion gene following chemotherapy and radiotherapy for breast cancer: A case report. Leukemia research reports 2 39258225
2014 The putative tumor suppressor ZMYND11 recognizes H3.3K36me3. Cancer discovery 2 24795016
2025 Zmynd11 is essential for neurogenesis by coordinating H3K36me3 modification of Epha2 and PI3K signaling pathway. Cell & bioscience 1 40281637
2024 ZMYND11 Functions in Bimodal Regulation of Latent Genes and Brain-like Splicing to Safeguard Corticogenesis. bioRxiv : the preprint server for biology 1 39464123
2026 Novel intermolecular zinc fingers and redox-driven conformational changes dictate tumor suppressor ZMYND11's role in cooperative recognition of diverse targets. Nucleic acids research 0 41591843
2026 A Complex Neurodevelopmental Phenotype Resembling a Chromatinopathy With Concurrent 7p Duplication and 10p Deletion Involving ZMYND11: A Case Report and Literature Review. Molecular genetics & genomic medicine 0 42003802
2025 ETS2 targets ZMYND11 to inhibit thyroid cancer progression via the mTOR signaling pathway. PloS one 0 40938895
2025 ZMYND11 Restrains KMT2A to Enable a Neuronal Developmental Program. bioRxiv : the preprint server for biology 0 41279818
2025 ZMYND11::MBTD1 Fusion in Myeloid/NK Cell Precursor Leukemia: A Case Report With Literature Review and Diagnostic Implications. Pediatric blood & cancer 0 41454826