Affinage

CHD3

ATP-dependent chromatin remodeler CHD3 · UniProt Q12873

Length
2000 aa
Mass
226.6 kDa
Annotated
2026-06-09
66 papers in source corpus 17 papers cited in narrative 17 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CHD3 is an ATP-dependent chromatin remodeler that serves as the monomeric catalytic ATPase subunit of isoform-specific NuRD (nucleosome remodeling and deacetylase) complexes, which it forms mutually exclusively with its paralog CHD4 and which differ in nucleosome remodeling behavior, nuclear localization, and target-gene regulation (PMID:28977666). Targeting is mediated by its tandem PHD fingers, which bind histone H3 tails with affinity enhanced by hydrophobicity-increasing modifications at H3K9 (H3K9me3 or H3K9ac), promoting nucleosome unwrapping and remodeling of pericentric heterochromatin (PMID:29020631). Its ATPase/helicase module couples ATP hydrolysis tightly to nucleosome translocation, such that basal hydrolysis suffices for remodeling, with translocation competitively inhibited by IP6 (PMID:33403747). In DNA double-strand break repair, CHD3 is recruited to breaks in a PARP1/poly(ADP-ribosyl)ation-dependent manner (PMID:29733391), and at heterochromatic breaks its dispersal is driven by ATM-dependent KAP-1 Ser824 phosphorylation, which disrupts the CHD3 SUMO-interacting motif–SUMO1 contact to permit chromatin relaxation and repair (PMID:21642969). Through NuRD, CHD3 controls developmental gene programs: it opens chromatin at BMP-responsive enhancers to drive BMP signalling and cranial neural crest specification, and its loss shifts cells toward aberrant mesodermal identity rescuable by Wnt titration (PMID:40835974). De novo missense mutations clustering in the ATPase/helicase domain reduce ATPase and chromatin remodeling activity and cause the neurodevelopmental disorder Snijders Blok-Campeau syndrome (PMID:30397230, PMID:41708849).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2003 Medium

    Established the first physical interaction partners of CHD3, mapping CGI-55 and Ki-1/57 to its C-terminal region and pointing to functions beyond the catalytic core.

    Evidence Yeast two-hybrid, in vitro pulldown, and Co-IP from Sf9 cells with GFP-fusion localization

    PMID:12505151

    Open questions at the time
    • Functional consequence of the CGI-55/Ki-1/57 interactions unresolved
    • No structural detail on the C-terminal binding interface
  2. 2007 Medium

    Showed that CHD3's C-terminus acts as a sequence-specific transcriptional repressor by partnering with the Ets factor ERM to silence the presenilin 1 promoter, demonstrating directed gene repression.

    Evidence Yeast two-hybrid interaction mapping, reporter assays, ChIP at the PS1 promoter, and deletion mutagenesis of CHD3 and ERM

    PMID:17489097

    Open questions at the time
    • Did not establish whether NuRD complex was required for repression
    • Generality beyond PS1 not addressed
  3. 2010 Medium

    Demonstrated in Drosophila that CHD3 acts as a monomeric remodeler associated with elongating RNA Pol II, raising the question of whether mammalian CHD3 is similarly complex-independent.

    Evidence Complex fractionation, in vitro chromatin remodeling, polytene chromosome immunofluorescence, and a viable/fertile deletion mutant

    PMID:20439780

    Open questions at the time
    • Dispensability in fly does not predict mammalian requirement
    • Mechanism linking CHD3 to Pol II elongation unexplored
  4. 2011 High

    Answered how heterochromatic DSB repair is licensed, showing ATM-driven KAP-1 Ser824 phosphorylation disrupts a CHD3 SIM–SUMO1 contact to disperse CHD3 and relax chromatin.

    Evidence Co-IP, mutagenesis of CHD3 SIM and KAP-1 Ser824, chromatin relaxation assays, and epistatic rescue of pKAP-1 requirement by CHD3 depletion

    PMID:21642969

    Open questions at the time
    • Does not address CHD3's catalytic role at euchromatic breaks
    • Whether SUMO1 contact is via the broader NuRD complex unresolved
  5. 2014 Medium

    Extended CHD3 function to host defense and viral hijacking, showing it represses HSV immediate-early genes via repressive histone marks yet is co-opted by influenza NS2 to promote vRNP nuclear export.

    Evidence Immunofluorescence, siRNA depletion, reporter assays, and NES1-mutagenesis Co-IP with viral propagation and export kinetics

    PMID:24425734 PMID:25213355

    Open questions at the time
    • Mechanism of CHD3 recognition of viral chromatin not detailed
    • Whether NuRD or CHD3 alone mediates these activities unclear
  6. 2017 High

    Defined CHD3 as the ATPase of a distinct NuRD complex (mutually exclusive with CHD4) and identified its PHD fingers as the H3K9me3/ac reader that directs remodeling to heterochromatin.

    Evidence MS proteomics, FRAP, HP1 Co-IP, UV-damage live imaging, peptide-binding and in vitro nucleosome unwrapping/remodeling assays with PHD mutants

    PMID:28977666 PMID:29020631

    Open questions at the time
    • Genome-wide division of labor between CHD3- and CHD4-NuRD incompletely mapped
    • Structural basis of PHD–H3K9 selectivity not solved
  7. 2018 High

    Connected CHD3 catalytic activity to human disease, showing ATPase/helicase-domain de novo mutations reduce ATPase and remodeling activity and cause Snijders Blok-Campeau syndrome, and clarified PARP-dependent recruitment to DSBs.

    Evidence Patient WGS cohort, structural modeling, in vitro ATPase and remodeling assays on six mutants; plus live-cell imaging with PARP inhibition for DSB recruitment

    PMID:29733391 PMID:30397230

    Open questions at the time
    • How specific mutations map to distinct neurodevelopmental features unresolved
    • PAR recruitment is not via direct PAR binding—intermediary unknown
  8. 2018 Medium

    Showed via the C. elegans orthologs CHD-3/LET-418 that NuRD-class Mi2 remodelers ensure faithful homologous-recombination DSB repair during meiosis, preventing toxic NHEJ-driven chromosomal fusions.

    Evidence Loss-of-function genetics, recombination-intermediate immunofluorescence, apoptosis quantification, and Mi2 × cku-80 epistasis

    PMID:29339410

    Open questions at the time
    • Worm ortholog—conservation of meiotic role in mammals not shown
    • Direct catalytic contribution versus complex role not separated
  9. 2020 Medium

    Established CHD3 as required for mammalian embryonic viability while demonstrating it does not cooperate with CHD4 in vascular development, reinforcing functional divergence between the paralogs.

    Evidence Conditional Chd3 knockout mice (Sox2-Cre and endothelial Cre), viability scoring, and double-deletion vascular epistasis

    PMID:32658897

    Open questions at the time
    • Tissue/cell type driving lethality not identified
    • Molecular basis of the requirement undefined
  10. 2021 High

    Resolved the enzymatic regulation of CHD3, showing tight ATP-hydrolysis-to-remodeling coupling (basal hydrolysis suffices) and competitive IP6 inhibition distinguishing it from SNF2H.

    Evidence Reconstituted in vitro ATPase and nucleosome translocation assays with conserved-motif mutagenesis and inhibitor dose-response

    PMID:33403747

    Open questions at the time
    • Physiological role of IP6 regulation in cells unknown
    • Structural basis of efficient coupling not determined
  11. 2025 High

    Demonstrated a developmental program in which CHD3-NuRD opens BMP-responsive enhancers to drive cranial neural crest specification, balancing BMP and Wnt signalling.

    Evidence CHD3-KO human iPSC differentiation with ATAC-seq, RNA-seq, ChIP-seq, and Wnt-level rescue

    PMID:40835974

    Open questions at the time
    • Direct enhancer targets versus indirect effects not fully separated
    • Relationship to Snijders Blok-Campeau craniofacial features not tested
  12. 2024 Medium

    Identified post-translational control of CHD3 abundance, showing FBW7-mediated ubiquitination and degradation restrains hepatocellular carcinoma aggressiveness and oxaliplatin resistance.

    Evidence Co-IP, ubiquitination assay, knockdown/overexpression rescue, and migration/invasion/stemness assays

    PMID:39473409

    Open questions at the time
    • Degron within CHD3 not mapped
    • Chromatin targets driving the oncogenic phenotype unidentified
  13. 2026 High

    Provided in vivo causal and therapeutic proof for CHD3 disease, with a humanized p.R1025W mouse recapitulating Snijders Blok-Campeau behavioural deficits that were reversed by in-brain adenine base editing, and revealed a context-specific cancer dependency via PARD3B enhancer repression.

    Evidence Humanized knock-in mice with dual-AAV base-editor delivery and behavioural rescue; plus CRISPR/siRNA depletion with ATAC/ChIP/RNA-seq and xenografts in SMARCA4/SMARCA2-deficient cancers

    PMID:41708849 PMID:42174139

    Open questions at the time
    • Durability and off-target profile of in vivo editing not fully resolved
    • Determinants of the synthetic-lethal CHD3 dependency in SWI/SNF-deficient tumors incompletely defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CHD3- versus CHD4-NuRD complexes are differentially assembled, targeted, and deployed across distinct cell types and developmental contexts remains the central open question.
  • No structure of full-length CHD3 within an intact NuRD complex
  • Rules governing isoform-specific genomic targeting unresolved
  • Mechanistic link between specific patient mutations and tissue phenotypes unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 3 GO:0140657 ATP-dependent activity 2 GO:0003677 DNA binding 1 GO:0016787 hydrolase activity 1 GO:0042393 histone binding 1
Localization
GO:0005634 nucleus 2 GO:0000228 nuclear chromosome 1
Pathway
R-HSA-1643685 Disease 4 R-HSA-4839726 Chromatin organization 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-73894 DNA Repair 2 R-HSA-1266738 Developmental Biology 1
Partners
CGI-55CHD4ERM/ETV5FBW7HP1KAP-1/TRIM28
Complex memberships
NuRD complex

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 ATM-dependent phosphorylation of KAP-1 at Ser824 generates a motif that directly perturbs the interaction between CHD3's SUMO-interacting motif (SIM) and SUMO1 on KAP-1, causing dispersal of CHD3 from heterochromatic DNA double-strand breaks (DSBs) and enabling chromatin relaxation and DSB repair. Depletion or inactivation of CHD3, or ablation of its interaction with KAP-1(SUMO1), bypassed the requirement for pKAP-1 in heterochromatic DSB repair. Co-immunoprecipitation, siRNA depletion, site-directed mutagenesis (CHD3 SIM mutant, KAP-1 Ser824 mutant), chromatin relaxation assays, epistasis (KAP-1 phospho-mutant rescue by CHD3 depletion) Nature structural & molecular biology High 21642969
2017 CHD3 and CHD4 form mutually exclusive, isoform-specific NuRD complexes (each complex contains either CHD3 or CHD4 as a monomeric ATPase subunit, not both). CHD3- and CHD4-NuRD complexes differ in nucleosome remodeling and positioning behavior in vitro, exhibit distinct nuclear localization patterns, and regulate overlapping but also distinct target genes. Both complexes interact with HP1 and accumulate at UV-induced DNA repair sites. Mass spectrometry-based proteomic mapping of NuRD subunit composition, FRAP (intranuclear mobility), Co-immunoprecipitation with HP1, live-cell imaging at UV damage sites, in vitro nucleosome remodeling assays Nucleic acids research High 28977666
2017 The tandem PHD fingers of CHD3 bind histone H3 tails, and post-translational modifications that increase hydrophobicity at H3K9 (H3K9me3 or H3K9ac) enhance this interaction. Binding of CHD3 PHDs promotes H3K9Cme3-nucleosome unwrapping in vitro and perturbs pericentric heterochromatin structure in vivo. H3K9 methylation or acetylation alleviates intra-nucleosomal interaction of H3 tails, increasing H3K9 accessibility for CHD3 binding. Peptide binding assays, in vitro nucleosome unwrapping assays, immunofluorescence/chromatin fractionation in cells (PHD mutants), ChIP co-localization with NuRD subunits Cell reports High 29020631
2018 De novo missense mutations clustering in the ATPase/helicase domain of CHD3 cause Snijders Blok-Campeau syndrome. Structural modeling shows these mutations disturb critical binding and interaction motifs. Experimental assays with six identified mutations showed a subset directly reduces ATPase activity, and all but one alter chromatin remodeling activity. Whole genome sequencing (patient cohort), 3D protein structural modeling, ATPase activity assays, chromatin remodeling assays (in vitro, six mutant variants tested) Nature communications High 30397230
2018 CHD3 is recruited to DNA double-strand breaks in a poly(ADP-ribosyl)ation-dependent manner (dependent on PARP1 activity), similar to CHD4, but not through direct PAR binding. Both CHD3 and CHD4 actively participate in chromatin remodeling at DNA breaks. An initial chromatin relaxation phase driven by PARP1 and Alc1/CHD1L promotes subsequent CHD3 and CHD4 recruitment via DNA binding for further remodeling. Live-cell fluorescence three-hybrid assay, laser micro-irradiation with live imaging, siRNA knockdown, PARP inhibitor treatment Nucleic acids research Medium 29733391
2014 CHD3 localizes to early herpes simplex virus (HSV) foci in infected cells, suppresses viral immediate early gene expression, and reduces the number of transcriptionally active viral genomes. CHD3 can recognize repressive histone marks associated with HSV chromatin. Depletion of CHD3 results in enhanced viral immediate early gene expression and increased numbers of transcriptionally active viral genomes. Immunofluorescence localization, siRNA depletion, reporter gene assays for viral immediate early gene expression, chromatin accessibility assays mBio Medium 24425734
2003 Two human proteins, CGI-55 and Ki-1/57, interact with the C-terminal region of CHD3 (residues after aa 1676). The CGI-55–CHD3 interaction was confirmed by yeast two-hybrid, in vitro pulldown, and co-immunoprecipitation from Sf9 insect cells. CGI-55 interacts with CHD3 via two regions at its N- and C-termini. Yeast two-hybrid, in vitro pulldown, co-immunoprecipitation from Sf9 cells, GFP-fusion localization FEBS letters Medium 12505151
2007 The C-terminal region of CHD3/ZFH (amino acids 1676–2000) interacts with the CIDD region (aa 96–349, critical residues 200–299) of the Ets transcription factor ERM, and this interaction represses transcription of the presenilin 1 (PS1) gene. CHD3 C-terminal fragment (aa 1676–2000) occupies the PS1 promoter in vivo. Sequences critical for repression and ERM binding are between aa 1862 and 1877 of CHD3. Yeast two-hybrid (interaction mapping), transfection reporter assays (transcription repression), chromatin immunoprecipitation (ChIP at PS1 promoter), deletion mutagenesis of both CHD3 and ERM The FEBS journal Medium 17489097
2014 CHD3 interacts with nuclear export signal 1 (NES1) of influenza A virus NS2 protein and co-localizes NS2 and Crm1 on dense chromatin to facilitate Crm1-dependent vRNP nuclear export. Disruption of the NS2–CHD3 interaction (by NES1 mutation) significantly delays vRNP export and viral propagation. CHD3 knockdown impairs propagation of wild-type virus but not a mutant with weakened NS2–CHD3 interaction. Co-immunoprecipitation, site-directed mutagenesis of NES1, siRNA knockdown of CHD3, viral propagation assays, nuclear export kinetics Cellular and molecular life sciences Medium 25213355
2021 The ATPase domain of CHD3 exhibits differential regulatory properties compared to SNF2H: IP6 inhibits CHD3 nucleosome translocation competitively (but not SNF2H), and CHD3 can translocate nucleosomes even at very low ATP concentrations. Mutations in conserved Q- and K-residues of the ATPase domain motifs show that basal ATP hydrolysis activity of CHD3 is sufficient for nucleosome remodeling (unlike SNF2H mutants), suggesting more efficient coupling of ATP hydrolysis and remodeling in CHD3. In vitro ATPase assays, nucleosome remodeling/translocation assays, site-directed mutagenesis of conserved ATPase motif residues, inhibitor dose-response (ADP, IP6) The FEBS journal High 33403747
2010 Drosophila CHD3 proteins act as monomers (not found in protein complexes) that remodel chromatin in vitro. Drosophila CHD3 co-localizes with elongating RNA polymerase II on salivary gland polytene chromosomes. Deletion of Chd3 has no effect on viability or fertility in Drosophila. Protein complex fractionation (monomeric vs. complex), in vitro chromatin remodeling assay, polytene chromosome immunofluorescence, targeted gene replacement (deletion mutant viability/fertility assay) Genetics Medium 20439780
2025 CHD3 (as a NuRD component) promotes BMP signalling during cranial neural crest cell (CNCC) specification by opening chromatin at BMP-responsive cis-regulatory elements and increasing expression of BMP-responsive transcription factors (including DLX paralogs). CHD3 loss leads to repression of BMP target genes, reduced chromatin accessibility at BMP-responsive enhancers, imbalance between BMP and Wnt signalling, and failure of CNCC specification replaced by aberrant mesodermal identity. This phenotype can be partially rescued by titrating Wnt levels. CHD3-KO human iPSC differentiation to CNCCs, ATAC-seq (chromatin accessibility), RNA-seq, ChIP-seq, Wnt-level rescue experiments EMBO reports High 40835974
2026 The recurrent CHD3 variant p.R1025W (modeled in humanized mice as Chd3hR1025W/+) reduces CHD3 protein levels and causes behavioural abnormalities including deficits in social communication, cognition and motor coordination recapitulating Snijders Blok-Campeau syndrome. In vivo adenine base editing (A•T-to-G•C correction) in the brain restored CHD3 protein levels and ameliorated these behavioural abnormalities. Humanized mouse knock-in model, in vivo dual-AAV delivery of adenine base editor (TeABE), behavioral phenotyping, western blot for CHD3 protein levels, on-target editing efficiency analysis across brain regions Nature High 41708849
2020 Conditional deletion of Chd3 throughout the epiblast results in partial lethality of homozygous Chd3Δ/Δ mice prior to weaning, establishing that CHD3 is required for embryonic viability. Endothelial-cell-specific deletion of Chd3 causes no vascular anomalies, and double-deletion of Chd3 and Chd4 in endothelial cells does not worsen CHD4-loss vascular phenotypes, indicating CHD3 does not cooperate with CHD4 in early vascular development. Conditional knockout mouse (floxed Chd3 allele, Sox2-Cre and endothelial Cre drivers), embryonic viability scoring, western blot for CHD3 protein, vascular phenotyping PloS one Medium 32658897
2024 FBW7 targets CHD3 for ubiquitination and proteasomal degradation. FBW7 overexpression suppresses HCC cell migration, invasion, stemness and oxaliplatin resistance; these effects are mediated through CHD3 ubiquitination, as overexpression of CHD3 rescues the FBW7-mediated suppression. Co-immunoprecipitation, ubiquitination assay, western blot, shRNA knockdown and overexpression rescue experiments, CCK-8/wound healing/transwell/sphere formation assays Frontiers in bioscience (Landmark edition) Medium 39473409
2026 In SMARCA4/SMARCA2 dual-deficient cancers, CHD3 (within the NuRD complex) acts as an essential epigenetic repressor at the PARD3B enhancer. Loss of CHD3 causes aberrant chromatin hyper-accessibility at the PARD3B enhancer, toxic derepression of PARD3B, attenuation of MYC signaling, and cell death. CHD3 depletion causes tumor regression in dual SMARCA4/SMARCA2-deficient xenografts. CRISPR/siRNA depletion of CHD3, ATAC-seq (chromatin accessibility at PARD3B enhancer), RNA-seq, ChIP-seq, in vivo xenograft experiments, integrated genomic analyses NPJ precision oncology Medium 42174139
2018 In C. elegans, the Mi2 homologs CHD-3 and its paralog LET-418 (components of the NuRD complex) facilitate meiotic progression by ensuring faithful DSB repair through homologous recombination. Loss of either CHD-3 or LET-418 results in elevated p53-dependent germ line apoptosis, activation of CHK-1, reduced offspring, persisting recombination intermediates in late pachytene nuclei, and chromosomal fusions due to inappropriate non-homologous end joining. C. elegans genetics (loss-of-function mutants), immunofluorescence for recombination intermediates, apoptosis quantification, double mutant analysis (Mi2 × cku-80 epistasis) Genetics Medium 29339410

Source papers

Stage 0 corpus · 66 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 Zfh-1 controls somatic stem cell self-renewal in the Drosophila testis and nonautonomously influences germline stem cell self-renewal. Cell stem cell 261 18593558
2011 KAP-1 phosphorylation regulates CHD3 nucleosome remodeling during the DNA double-strand break response. Nature structural & molecular biology 211 21642969
1991 The embryonic expression patterns of zfh-1 and zfh-2, two Drosophila genes encoding novel zinc-finger homeodomain proteins. Mechanisms of development 165 1680377
1991 The Drosophila zfh-1 and zfh-2 genes encode novel proteins containing both zinc-finger and homeodomain motifs. Mechanisms of development 154 1680376
2012 The CHD3 remodeler PICKLE associates with genes enriched for trimethylation of histone H3 lysine 27. Plant physiology 128 22452853
2000 Differential expression and function of members of the zfh-1 family of zinc finger/homeodomain repressors. Proceedings of the National Academy of Sciences of the United States of America 125 10841546
1997 ZEB, a vertebrate homolog of Drosophila Zfh-1, is a negative regulator of muscle differentiation. The EMBO journal 125 9233803
2008 The CHD3 remodeler PICKLE promotes trimethylation of histone H3 lysine 27. The Journal of biological chemistry 112 18539592
1998 zfh-1 is required for germ cell migration and gonadal mesoderm development in Drosophila. Development (Cambridge, England) 102 9435286
2018 CHD3 helicase domain mutations cause a neurodevelopmental syndrome with macrocephaly and impaired speech and language. Nature communications 94 30397230
1993 Loss of function of the Drosophila zfh-1 gene results in abnormal development of mesodermally derived tissues. Proceedings of the National Academy of Sciences of the United States of America 93 8097886
2017 CHD3 and CHD4 form distinct NuRD complexes with different yet overlapping functionality. Nucleic acids research 92 28977666
2012 CHD3 protein recognizes and regulates methylated histone H3 lysines 4 and 27 over a subset of targets in the rice genome. Proceedings of the National Academy of Sciences of the United States of America 88 22451926
1999 zfh-1, the Drosophila homologue of ZEB, is a transcriptional repressor that regulates somatic myogenesis. Molecular and cellular biology 86 10490660
1999 The Drosophila homeobox genes zfh-1 and even-skipped are required for cardiac-specific differentiation of a numb-dependent lineage decision. Development (Cambridge, England) 74 10375513
2012 Revealing the stereospecific chemistry of the reaction of Cl with aligned CHD₃(ν₁ = 1). Nature chemistry 69 22824895
2018 CHD3 and CHD4 recruitment and chromatin remodeling activity at DNA breaks is promoted by early poly(ADP-ribose)-dependent chromatin relaxation. Nucleic acids research 59 29733391
2003 Characterization of a new family of proteins that interact with the C-terminal region of the chromatin-remodeling factor CHD-3. FEBS letters 55 12505151
2017 Covalent Modifications of Histone H3K9 Promote Binding of CHD3. Cell reports 38 29020631
2020 A second cohort of CHD3 patients expands the molecular mechanisms known to cause Snijders Blok-Campeau syndrome. European journal of human genetics : EJHG 37 32483341
1995 Expression of zfh-4, a new member of the zinc finger-homeodomain family, in developing brain and muscle. Developmental dynamics : an official publication of the American Association of Anatomists 36 7537552
2015 CHR729 Is a CHD3 Protein That Controls Seedling Development in Rice. PloS one 34 26398683
2019 Wheat CHD3 protein TaCHR729 regulates the cuticular wax biosynthesis required for stimulating germination of Blumeria graminis f.sp. tritici. Journal of experimental botany 33 30364999
2019 Mutations in the Rice OsCHR4 Gene, Encoding a CHD3 Family Chromatin Remodeler, Induce Narrow and Rolled Leaves with Increased Cuticular Wax. International journal of molecular sciences 28 31130602
2008 Divergent evolution of CHD3 proteins resulted in MOM1 refining epigenetic control in vascular plants. PLoS genetics 26 18725928
2022 Inherited variants in CHD3 show variable expressivity in Snijders Blok-Campeau syndrome. Genetics in medicine : official journal of the American College of Medical Genetics 23 35346573
2014 CHD3 facilitates vRNP nuclear export by interacting with NES1 of influenza A virus NS2. Cellular and molecular life sciences : CMLS 22 25213355
2000 Kheper, a novel ZFH/deltaEF1 family member, regulates the development of the neuroectoderm of zebrafish (Danio rerio). Developmental biology 22 11087624
2018 The Rice Rolled Fine Striped (RFS) CHD3/Mi-2 Chromatin Remodeling Factor Epigenetically Regulates Genes Involved in Oxidative Stress Responses During Leaf Development. Frontiers in plant science 21 29616070
2018 Dissociation of CHD3 on Cu(111), Cu(211), and single atom alloys of Cu(111). The Journal of chemical physics 19 30553257
2000 The mouse ZFH-4 protein contains four homeodomains and twenty-two zinc fingers. Biochemical and biophysical research communications 19 10873665
2022 Vibrational control of the reaction pathway in the H + CHD3 → H2 + CD3 reaction. Science advances 18 35353570
2018 Maintenance of Genome Integrity by Mi2 Homologs CHD-3 and LET-418 in Caenorhabditis elegans. Genetics 17 29339410
2014 Epigenetic repression of herpes simplex virus infection by the nucleosome remodeler CHD3. mBio 17 24425734
2014 Differential expression and sex chromosome association of CHD3/4 and CHD5 during spermatogenesis. PloS one 16 24849318
2005 Novel transcription factor zfh-5 is negatively regulated by its own antisense RNA in mouse brain. Molecular and cellular neurosciences 16 16257534
2007 Differentiation of the Drosophila serotonergic lineage depends on the regulation of Zfh-1 by Notch and Eagle. Molecular and cellular neurosciences 14 17702602
2003 Embryonic enhancers in the dpp disk region regulate a second round of Dpp signaling from the dorsal ectoderm to the mesoderm that represses Zfh-1 expression in a subset of pericardial cells. Developmental biology 14 14512024
2021 Hypersociability associated with developmental delay, macrocephaly and facial dysmorphism points to CHD3 mutations. European journal of medical genetics 12 33571694
2020 A de novo CHD3 variant in a child with intellectual disability, autism, joint laxity, and dysmorphisms. Brain & development 12 33358638
2014 Correlated Dynamics of the O((3)P) + CHD3(v=0) Reaction: A Joint Crossed-Beam and Quasiclassical Trajectory Study. The journal of physical chemistry. A 12 25455856
2010 Molecular genetic analysis of Chd3 and polytene chromosome region 76B-D in Drosophila melanogaster. Genetics 10 20439780
2021 Zfh-2 facilitates Notch-induced apoptosis in the CNS and appendages of Drosophila melanogaster. Developmental biology 9 33705738
2023 Snijders Blok-Campeau Syndrome: Description of 20 Additional Individuals with Variants in CHD3 and Literature Review. Genes 7 37761804
2022 A novel CHD3 variant in a patient with central precocious puberty: Expanded phenotype of Snijders Blok-Campeau syndrome? American journal of medical genetics. Part A 7 36565043
2011 Restricted expression of chromatin remodeling associated factor Chd3 during tooth root development. Journal of periodontal research 7 21972924
2020 The chromatin-remodeling enzyme CHD3 plays a role in embryonic viability but is dispensable for early vascular development. PloS one 6 32658897
2007 The C-terminal region of CHD3/ZFH interacts with the CIDD region of the Ets transcription factor ERM and represses transcription of the human presenilin 1 gene. The FEBS journal 6 17489097
2024 Novel genotypes and phenotypes in Snijders Blok-Campeau syndrome caused by CHD3 mutations. Frontiers in genetics 5 39050258
2021 Snijders Blok-Campeau syndrome caused by CHD3 gene mutation: a case report. Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics 5 34535214
2024 FBW7-Mediated Degradation of CHD3 Suppresses Hepatocellular Carcinoma Metastasis and Stemness to Enhance Oxaliplatin Sensitivity. Frontiers in bioscience (Landmark edition) 4 39473409
2023 A severe neurocognitive phenotype caused by biallelic CHD3 variants in two siblings. American journal of medical genetics. Part A 3 38116750
2026 In vivo base editing of Chd3 rescues behavioural abnormalities in mice. Nature 2 41708849
2025 The NuRD component CHD3 promotes BMP signalling during cranial neural crest cell specification. EMBO reports 2 40835974
2024 Insights From a Novel Splicing Variant and Recurrent Arginine Variants in the CHD3 Gene Causing Snijders Blok-Campeau Syndrome. American journal of medical genetics. Part A 2 39542866
2021 The Rice CHD3/Mi-2 Chromatin Remodeling Factor Rolled Fine Striped Promotes Flowering Independent of Photoperiod. International journal of molecular sciences 2 33525623
2020 Combined in silico analysis identified a putative tooth root formation-related gene, Chd3, which regulates DNA synthesis in HERS01a cells. Odontology 2 32026140
2026 A conserved C. elegans zinc finger homeodomain protein, ZFH-2, is continuously required for the structural integrity and function of the alimentary tract and gonad. Development (Cambridge, England) 1 41954129
2025 Neurobehavioral profile of individuals with pathogenic variants in CHD3. European journal of human genetics : EJHG 1 40830229
2026 A conserved C. elegans zinc finger-homeodomain protein, ZFH-2, continuously required for structural integrity and function of alimentary tract and gonad. bioRxiv : the preprint server for biology 0 41648380
2026 Identification of an episignature for CHD3-related Snijders Blok-Campeau syndrome reveals heterogeneity in the CHARGE syndrome episignature: towards a better characterisation of chromatinopathies. Genome medicine 0 41952182
2026 Targeting the CHD3 chromatin remodeler exploits a synthetic lethal vulnerability in dual SMARCA4/SMARCA2-deficient cancers via derepression of PARD3B. NPJ precision oncology 0 42174139
2025 Infantile spasm, an unreported epilepsy form of CHD3 gene: A case report. Medicine 0 40527848
2024 Rice CHD3/Mi-2 chromatin remodeling factor RFS regulates vascular development and root formation by modulating the transcription of auxin-related genes NAL1 and OsPIN1. BMB reports 0 39044456
2024 CHD3-related Snijders Blok-Campeau syndrome with Spastic Paraplegia, Ataxia, and Situs Inversus. European journal of medical genetics 0 39709005
2021 Sequence and functional differences in the ATPase domains of CHD3 and SNF2H promise potential for selective regulability and drugability. The FEBS journal 0 33403747

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