Affinage

KAT6B

Histone acetyltransferase KAT6B · UniProt Q8WYB5

Length
2073 aa
Mass
231.4 kDa
Annotated
2026-06-10
100 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/5 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KAT6B (MORF/QKF/MYST4) is a MYST-family lysine acetyltransferase that operates as the catalytic core of a tetrameric complex with BRPF1/2/3, ING5, and EAF6, in which BRPF1 bridges complex assembly and drastically stimulates acetyltransferase activity toward nucleosomal H3 and free histones H3 and H4 (PMID:18794358). The native complex is an H3K23-specific acetyltransferase whose chromatin engagement is governed by reader and DNA-binding modules: the DPF (double PHD finger) domain recognizes lipophilic acyllysine marks such as crotonylated and butyrylated H3K14 to promote H3K23 acetylation of target genes (PMID:31624313, PMID:28286003), the tandem PHD fingers bind the H3 N-terminal tail (enhanced by H3K9/H3K14 acetylation, inhibited by H3K4me3) to direct chromatin localization (PMID:23063713), and tandem winged-helix domains WH1/WH2 bind unmethylated CpG DNA and the nucleosome dyad cooperatively to target promoters and stimulate transcription and H3K23 acetylation, with WH1 additionally engaging the p300 TAZ2 domain to coordinate with p300-driven H3K18 acetylation (PMID:36754959, PMID:38500836). Through its C-terminal SM domain, KAT6B physically binds and coactivates the Runt-domain transcription factors Runx2 and Runx1 without acetylating them (PMID:11965546). KAT6B is essential for cortical neurogenesis and adult neural stem cell self-renewal (PMID:10821753, PMID:17079664) and for hematopoietic stem cell function, where it sustains H3K9 acetylation and, in cooperation with the paralog KAT6A, drives transcription of hematopoietic regulators including the Hoxa cluster, Pbx1, Meis1, and Gata genes; sufficiently high KAT6B expression fully substitutes for KAT6A (PMID:38518784, PMID:40000651). KAT6B loss de-represses RUNX2-driven osteoblast differentiation to cause premature ossification (PMID:39832706) and reduces H3K9 acetylation with dysregulated MAPK signaling (PMID:21804188); human loss-of-function mutations cause genitopatellar and SBBYSS intellectual-disability syndromes, and elevating histone acetylation pharmacologically partially reverses neurological deficits in Kat6b-deficient mice (PMID:22265017, PMID:38557491).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2000 High

    Established KAT6B as an essential developmental regulator by showing it is required for cerebral cortex differentiation, before any biochemical activity was assigned.

    Evidence Gene-trap mouse mutagenesis with histological and immunostaining analysis of cortical layers

    PMID:10821753

    Open questions at the time
    • Did not define the molecular activity underlying the phenotype
    • No chromatin or substrate-level mechanism
  2. 2002 High

    Connected KAT6B to a transcriptional program by demonstrating its SM domain binds and coactivates Runx2/Runx1, defining a non-catalytic transcription-factor partnership.

    Evidence In vitro binding, co-IP, reporter assays, and knockdown in cells

    PMID:11965546

    Open questions at the time
    • KAT6B does not acetylate Runx2, so the molecular basis of coactivation is unresolved
    • Did not connect to histone acetylation at Runx target genes
  3. 2006 High

    Extended the developmental role to adult tissue by showing KAT6B sustains neural stem cell self-renewal and neuroblast production.

    Evidence Hypomorphic mouse model, in vivo cell counting, neurosphere self-renewal and differentiation assays

    PMID:17079664

    Open questions at the time
    • Did not identify direct target genes in neural stem cells
    • Molecular mechanism of self-renewal control unknown
  4. 2008 High

    Defined the biochemical core of KAT6B function by reconstituting the BRPF1/ING5/EAF6 tetramer and showing BRPF1 bridges assembly and drastically stimulates HAT activity on nucleosomes.

    Evidence Reconstituted complexes, deletion mapping, in vitro HAT assays, co-IP, reporter assays

    PMID:18794358

    Open questions at the time
    • Did not pinpoint a single primary histone-lysine substrate
    • In vivo genomic targets of the complex not mapped
  5. 2011 High

    Linked KAT6B haploinsufficiency to a signaling defect, showing reduced H3 acetylation hyperactivates MAPK during morphogenesis.

    Evidence Breakpoint mapping, H3 acetylation assays, ChIP, expression profiling, siRNA, querkopf mouse

    PMID:21804188

    Open questions at the time
    • Direct vs indirect control of MAPK genes not fully separated
    • Specific acetylated lysine not yet resolved
  6. 2012 High

    Resolved how the complex recognizes chromatin, showing tandem PHD fingers read the H3 tail with acetylation-enhanced and H3K4me3-inhibited binding required for localization.

    Evidence NMR, fluorescence spectroscopy, mutagenesis, IP, microscopy, in vitro HAT assay

    PMID:23063713

    Open questions at the time
    • How PHD reading couples to catalytic stimulation in trans not fully defined
  7. 2012 Medium

    Confirmed human disease causality by tying GPS-causing truncating mutations to reduced H3/H4 acetylation in patient cells.

    Evidence Exome/Sanger sequencing and histone acetylation assays in patient-derived cells

    PMID:22265017

    Open questions at the time
    • No pathway dissection beyond global histone modification
    • Genome-wide target consequences not mapped
  8. 2017 High

    Provided structural basis for acyl-mark reading, showing the DPF domain selects lipophilic H3K14 acylations (butyryl) to support spreading of acylation.

    Evidence Crystal structure of DPF-H3K14butyryl, mass spectrometry, binding assays

    PMID:28286003

    Open questions at the time
    • Functional consequence of acyl reading on genomic targets shown later, not here
  9. 2019 High

    Established H3K23 as the principal substrate of the native complex and tied catalysis to DPF reading of crotonylated H3K14.

    Evidence Native complex HAT assay, DPF-H3K14cr crystal structure, mass spectrometry, ChIP-seq

    PMID:31624313

    Open questions at the time
    • Relationship between H3K23ac and H3K9ac substrate preference across cell types unresolved
  10. 2019 Medium

    Connected KAT6B to chromatin architecture and pluripotency by showing its loss compacts chromatin and impairs Oct4/Nanog-chromatin binding in ES cells.

    Evidence CRISPR KO ES cells, fluorescence correlation spectroscopy, neural differentiation

    PMID:30790630

    Open questions at the time
    • Direct vs indirect effect on Oct4/Nanog binding not separated
    • Histone substrate at affected loci not defined
  11. 2023 High

    Defined the DNA-targeting mechanism, showing tandem winged-helix domains cooperatively bind unmethylated CpG and the nucleosome dyad to direct the complex to promoters.

    Evidence Cryo-EM, NMR, mass spectrometry, mutagenesis, ChIP-seq, transcriptional assays

    PMID:36754959

    Open questions at the time
    • How WH targeting integrates with PHD/DPF reading at native loci not fully reconstructed
  12. 2024 Medium

    Revealed coordination with a second acetyltransferase, showing WH1 binds the p300 TAZ2 domain and co-localizes with p300-deposited H3K18ac at CpG promoters.

    Evidence Biochemical structural analysis, ChIP-seq, binding assays

    PMID:38500836

    Open questions at the time
    • Direct functional cooperation in vivo not demonstrated by epistasis
    • Single lab
  13. 2024 High

    Refined the hematopoietic substrate and revealed paralog redundancy, showing KAT6B maintains H3K9ac (not H3K23ac) in HSCs and cooperates with KAT6A to drive hematopoietic gene programs.

    Evidence KO/OE and compound-heterozygote mouse models, histone acetylation assays, transplantation, transcriptome

    PMID:38518784

    Open questions at the time
    • Why substrate preference differs from H3K23ac in other systems unresolved
    • Direct vs indirect regulation of Hoxa/Meis1 not fully separated
  14. 2024 High

    Established a therapeutic rationale for the neurological syndrome, showing H3K9ac loss in SBBYSS cells/mice is partially reversed pharmacologically with behavioral rescue.

    Evidence Kat6b+/- mouse, human SBBYSS cells, H3K9ac assays, HDAC inhibitor/ALCAR treatment, behavior, transcriptome

    PMID:38557491

    Open questions at the time
    • Direct target genes mediating behavioral rescue not pinpointed
    • Durability of rescue not addressed
  15. 2025 High

    Placed KAT6B upstream of RUNX2 in skeletal development by genetic epistasis, explaining premature ossification as RUNX2 de-repression.

    Evidence Germline Kat6b deletion mouse, Kat6b x Runx2 compound heterozygote rescue, histology, transcriptome

    PMID:39832706

    Open questions at the time
    • Molecular step by which KAT6B restrains RUNX2 targets not defined
    • Relationship to the earlier SM-domain Runx2 coactivation not reconciled
  16. 2025 High

    Demonstrated full functional overlap with KAT6A, showing KAT6B overexpression rescues all defects of Kat6a-null mice including HSC loss and restores H3K9ac/H3K23ac.

    Evidence Transgenic Kat6b overexpression in Kat6a-null background, histone acetylation assays, transcriptome, reconstitution

    PMID:40000651

    Open questions at the time
    • Endogenous division of labor between paralogs under physiological dosage not resolved
  17. 2025 Medium

    Showed dosage sensitivity in the nervous system, with KAT6B overexpression elevating H3K9ac, biasing neuronal differentiation, and producing behavioral/epileptic phenotypes.

    Evidence Transgenic Kat6b overexpression mouse, behavior, H3K9ac assays, NSC differentiation assays, transcriptome

    PMID:40083716

    Open questions at the time
    • Direct target genes driving behavioral phenotypes not defined
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How KAT6B's chromatin-reading and DNA-targeting modules integrate to select H3K9 versus H3K23 acetylation in a cell-type-specific manner, and how this dictates distinct neural, skeletal, and hematopoietic programs, remains unresolved.
  • Determinants of H3K9ac vs H3K23ac substrate choice across tissues unknown
  • Unified model linking SM-domain TF coactivation, WH/PHD/DPF chromatin targeting, and disease phenotypes lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 5 GO:0003677 DNA binding 3 GO:0042393 histone binding 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0140110 transcription regulator activity 3
Localization
GO:0000228 nuclear chromosome 2 GO:0005634 nucleus 2
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-4839726 Chromatin organization 3 R-HSA-74160 Gene expression (Transcription) 3
Partners
BRPF1EAF6EP300ING5RUNX1RUNX2
Complex memberships
KAT6B-BRPF1/2/3-ING5-EAF6 MYST acetyltransferase complex

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 MORF (KAT6B) forms tetrameric complexes with ING5, EAF6, and BRPF1/2/3. BRPF1 bridges the association of MORF with ING5 and EAF6 via its N-terminal region (acetyltransferase domain interaction) and EPc homology domain (ING5/EAF6 interaction). Complex formation with BRPF1 and ING5 drastically stimulates MORF acetyltransferase activity on nucleosomal histone H3 and free histones H3 and H4. An 18-residue 'activation lid' at the C-terminal end of the catalytic domain is required for BRPF1 interaction. Reconstitution of tetrameric complexes, deletion mapping, in vitro HAT assays on nucleosomal and free histones, co-immunoprecipitation, reporter transcription assays Molecular and cellular biology High 18794358
2002 MORF (KAT6B) physically interacts with the Runt-domain transcription factor Runx2 (and Runx1/AML1) through its C-terminal SM (serine- and methionine-rich) domain, both in vitro and in vivo. The SM domain of MORF potentiates Runx2-dependent transcriptional activation, and endogenous MORF is required for transcriptional activation by Runx2. MORF does not acetylate Runx2. Runx2 negatively regulates the transcriptional activation potential of the SM domain. In vitro binding assay, co-immunoprecipitation (in vivo), reporter transcription assay, siRNA/dominant-negative knockdown Oncogene High 11965546
2000 KAT6B (Querkopf/Qkf) is required for normal cerebral cortex development in mice. Homozygous querkopf mutants show a disproportionately small cortical plate, lack of large pyramidal cells in cortical layer V (reduced Otx1-positive neurons), and reduced GAD67-positive interneurons, establishing KAT6B as an essential regulator of cortical cell differentiation. Gene trap mouse mutagenesis, histological and immunostaining analysis of cortical layers Development (Cambridge, England) High 10821753
2006 KAT6B (Qkf) is essential for adult neurogenesis. Qkf-deficient mice have fewer neural stem cells, fewer migrating neuroblasts in the rostral migratory stream, and declining numbers of olfactory bulb interneurons. Neural stem/progenitor cells from Qkf mutant mice show reduced self-renewal and reduced ability to produce differentiated neurons. Qkf hypomorphic mouse model, in vivo cell counting, neurosphere self-renewal assay, differentiation assays from isolated stem/progenitor cells The Journal of neuroscience High 17079664
2011 Haploinsufficiency of KAT6B (MYST4) in a patient with Noonan syndrome-like phenotype leads to reduced H3 acetylation and hyperactivation of the MAPK signaling pathway. ChIP and whole-genome expression studies in patient cells and siRNA knockdown cell lines showed that H3 acetylation by KAT6B specifically regulates the MAPK signaling pathway during neural, craniofacial, and skeletal morphogenesis. Chromosomal breakpoint mapping, H3 acetylation assays, ChIP, whole genome expression analysis, siRNA knockdown in cell lines, Myst4 querkopf mouse The Journal of clinical investigation High 21804188
2012 GPS-causing KAT6B truncating mutations result in reduced histone H3 and H4 acetylation in patient-derived cells, directly linking KAT6B loss-of-function to dysregulation of histone acetylation. Exome sequencing, Sanger sequencing, histone acetylation assays in patient-derived cells American journal of human genetics Medium 22265017
2019 The native MORF (KAT6B) complex is a histone H3K23-specific acetyltransferase. The DPF (double PHD finger) domain of MORF (MORFDPF) positively regulates MORF acetyltransferase function by recognizing crotonylated H3K14; crystal structure of MORFDPF-H3K14crotonyl complex reveals selectivity for lipophilic acyllysine substrates and DNA binding. ChIP data show that MORFDPF is required for MORF-dependent H3K23 acetylation of target genes. Mass spectrometry and genomic analyses demonstrate co-existence and co-occupancy of H3K23ac and H3K14ac marks. Native complex purification, in vitro HAT assay, crystal structure of DPF-H3K14 crotonyl peptide complex, mass spectrometry, ChIP-seq, biochemical binding assays Nature communications High 31624313
2017 The DPF domain of MORF (KAT6B) recognizes many histone H3K14 acylation marks (including butyrylation). Crystal structure of the MORF DPF-H3K14butyryl complex provides insight into selectivity for lipophilic acyllysine substrates, supporting a mechanism by which MORF promotes spreading of histone acylation. Crystal structure determination, mass spectrometry, in vitro binding assays Structure (London, England : 1993) High 28286003
2012 The tandem PHD1/2 fingers of MORF (KAT6B) recognize the N-terminal tail of histone H3; acetylation of H3K9 or H3K14 enhances binding 2-3 fold. Trimethylation of H3K4 inhibits the interaction. NMR, fluorescence spectroscopy, and mutagenesis identified key residues. Both PHD fingers are required for binding H3K14ac in vivo and for chromatin localization. H3K14ac interaction may promote MORF enzymatic activity in trans. NMR, fluorescence spectroscopy, mutagenesis, immunoprecipitation, fluorescence microscopy, in vitro HAT assay Journal of molecular biology High 23063713
2023 MORF (KAT6B) and MOZ contain two structured winged helix (WH) domains (WH1 and WH2). WH1 specifically recognizes unmethylated CpG sequences and WH2 binds the dyad of the nucleosome. WHs bind DNA cooperatively and target MORF/MOZ to gene promoters, stimulating transcription and H3K23 acetylation. WH1 recruits oncogenic fusions to HOXA genes. Cryo-EM, NMR, mass spectrometry, and mutagenesis provided mechanistic insight. Cryo-EM structure, NMR, mass spectrometry, mutagenesis, ChIP-seq, transcriptional assays Nature communications High 36754959
2024 The first winged helix domain of MORF (MORFWH1) has dual binding activity: it recognizes the TAZ2 domain of p300 and CpG-rich DNA sequences through distinct binding sites. MORF/MOZWH1 co-localizes with H3K18ac (a product of p300 enzymatic activity) on CpG-rich promoters of target genes, suggesting functional cooperation of MORF and p300 acetyltransferases in transcriptional regulation. Structural analysis (biochemical), ChIP-seq genomic analysis, binding assays iScience Medium 38500836
2015 KAT6B acts as a tumor suppressor in small cell lung cancer through histone H3 Lys23 acetyltransferase activity. Homozygous deletions of KAT6B are present in SCLC cell lines and primary tumors. Depletion of KAT6B enhances cancer cell growth in vitro and in vivo, while restoration induces tumor suppressor-like features. Genomic deletion analysis, KAT6B knockdown/restoration in cell lines and xenograft mouse models, in vitro HAT assay for H3K23 Cancer research Medium 26208904
2019 KAT6B (MORF) regulates chromatin organization and modulates binding of pluripotency transcription factors Oct4 and Nanog to chromatin in embryonic stem cells. Kat6b knockout (CRISPR/Cas9) ES cells show more compact chromatin organization (fluorescence correlation spectroscopy) and impaired Oct4/Nanog-chromatin interactions, and exhibit reduced efficiency of neural lineage differentiation. Kat6b is expressed in ES cells and is repressed during differentiation; its expression is regulated by Nanog and Oct4. CRISPR/Cas9 knockout ES cells, fluorescence correlation spectroscopy, neural differentiation assay Journal of molecular biology Medium 30790630
2020 KAT6B regulates hematopoietic stem cell (HSC) myeloid differentiation. Kat6b is highly expressed in long-term HSCs and decreases with aging. Knockdown of Kat6b in young LT-HSCs causes skewed myeloid production at the expense of erythroid cells in vitro and in vivo, with upregulation of aging/macrophage gene signatures and downregulation of self-renewal signatures. shRNA screen, in vitro and in vivo differentiation assays after knockdown, transcriptome analysis Experimental hematology Medium 32014431
2024 KAT6B is essential for normal levels of histone H3 lysine 9 (H3K9) acetylation (but not H3K23 as previously proposed) in hematopoietic stem cells. Compound heterozygosity of Kat6b and Kat6a abolishes hematopoietic reconstitution after transplantation. KAT6B and KAT6A cooperatively promote transcription of hematopoiesis-regulating genes including Hoxa cluster, Pbx1, Meis1, Gata family, Erg, and Flt3. Germline deletion and overexpression mouse models, histone acetylation assays, bone marrow transplantation, transcriptome analysis, compound heterozygote analysis Stem cell reports High 38518784
2024 KAT6B deficiency causes reduction in histone H3 lysine 9 acetylation (H3K9ac) in human SBBYSS cells and mouse brain/blood. Treatment with HDAC inhibitor (valproic acid) or acetyl-carnitine (ALCAR) elevated histone acetylation levels and partially reversed gene expression changes in Kat6b+/- cortical neurons, improving sociability and restoring learning and memory in Kat6b+/- mice. Kat6b heterozygous mouse model, human SBBYSS patient cells, H3K9ac assays, HDAC inhibitor treatment, behavioral assays, cortical neuron transcriptome The Journal of clinical investigation High 38557491
2025 KAT6B loss of function in mesenchymal progenitor cells promotes transition toward an osteoblast-progenitor state with upregulation of RUNX2 gene targets and downregulation of SOX9. Compound heterozygosity at Kat6b and Runx2 loci partially rescues the ossification deficit of Runx2 heterozygous mice, placing KAT6B upstream of RUNX2 in limiting osteoblast differentiation. KAT6B loss causes premature ossification, shortened craniofacial elements, increased bone density, and shortened tibias. Germline Kat6b deletion mouse, compound heterozygote genetic epistasis (Kat6b x Runx2), histology, transcriptome analysis, immunostaining Developmental biology High 39832706
2025 4-fold overexpression of Kat6b rescues all developmental defects in Kat6a homozygous null mice, including absence of hematopoietic stem cells. Kat6b overexpression restores H3K9 and H3K23 acetylation and reverses critical gene expression anomalies in Kat6a mutant mice, demonstrating functional overlap between KAT6B and KAT6A when KAT6B is expressed at sufficiently high levels. Transgenic Kat6b overexpression in Kat6a null mouse background, histone acetylation assays (H3K9ac, H3K23ac), transcriptome analysis, hematopoietic reconstitution assays Nature communications High 40000651
2016 Decreased KAT6B (MORF) expression in periodontitis-associated mesenchymal stem cells causes upregulation of PERK (a key UPR sensor), leading to persistent UPR activation and impaired osteogenic differentiation. KAT6B mediates PERK transcription; chronic inflammation suppresses KAT6B, thereby compromising UPR function through MORF-mediated PERK transcriptional regulation. Cell culture with proinflammatory cytokines, KAT6B knockdown/overexpression, in vivo periodontitis model, PERK and osteogenic differentiation assays Cell death and differentiation Medium 27447113
2017 KAT6B promotes LPS-triggered IL-6 production in macrophages by increasing recruitment of H3K23 acetylation to the IL-6 gene promoter region. KAT6B knockdown suppressed LPS-induced IL-6 production; KAT6B overexpression promoted it. The effect was not mediated through changes in NF-κB p65 or MAPK activity. siRNA knockdown, overexpression, qRT-PCR, ELISA, ChIP (H3K23ac at IL-6 promoter), dual-luciferase reporter assay, Western blot Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology Medium 29268844
2025 KAT6B overexpression in mice causes aggression, anxiety, and spontaneous epilepsy. Kat6b overexpression increases histone H3K9 acetylation and upregulates genes driving nervous system development and neuronal differentiation. KAT6B overexpression promotes neural stem cell proliferation and favors neuronal over astrocyte differentiation in vivo and in vitro. Transgenic Kat6b overexpression mouse, behavioral assays, H3K9ac assays, neural stem cell differentiation assays in vivo and in vitro, transcriptome iScience Medium 40083716
2013 KAT6B silencing in prostate cancer DU145 cells suppresses AKT signaling (PI3K-AKT pathway), reducing cell proliferation. DNA microarray and IPA analysis identified PI3K signaling among suppressed pathways upon KAT6B knockdown. RNAi screen, gene-specific siRNA knockdown, DNA microarray, Ingenuity Pathway Analysis, immunoblotting for AKT International journal of clinical and experimental pathology Low 24294372
2022 KAT6B occupies the STAT3 promoter in glioma cells and promotes H3K23 acetylation (H3K23ac) and RNA polymerase II enrichment at the STAT3 promoter, thereby transcriptionally activating STAT3. KAT6B knockdown reduces H3K23ac and RNA pol II at the STAT3 promoter and downregulates STAT3, suppressing ferroptosis resistance. ChIP assay (H3K23ac and RNA pol II at STAT3 promoter), KAT6B knockdown/overexpression, cell viability and apoptosis assays Journal of oncology Low 35432536
2007 MYST4 (KAT6B) protein is expressed in specialized reproductive cells: in the ovary it is confined to oocytes, granulosa and theca cells, and vascular cells; in the testis it is restricted to elongating spermatids where it is exclusively nuclear. In oocytes and embryos, MYST4 protein localizes to both cytoplasm and nucleus. Immunohistochemistry on ovary and testis sections, subcellular localization by immunostaining in oocytes/embryos BMC developmental biology Low 17980037

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Multiple organellar RNA editing factor (MORF) family proteins are required for RNA editing in mitochondria and plastids of plants. Proceedings of the National Academy of Sciences of the United States of America 247 22411807
2008 Molecular architecture of quartet MOZ/MORF histone acetyltransferase complexes. Molecular and cellular biology 193 18794358
2001 Fusion of the MORF and CBP genes in acute myeloid leukemia with the t(10;16)(q22;p13). Human molecular genetics 164 11157802
2011 Whole-exome-sequencing identifies mutations in histone acetyltransferase gene KAT6B in individuals with the Say-Barber-Biesecker variant of Ohdo syndrome. American journal of human genetics 153 22077973
2002 MOZ and MORF histone acetyltransferases interact with the Runt-domain transcription factor Runx2. Oncogene 137 11965546
2000 Querkopf, a MYST family histone acetyltransferase, is required for normal cerebral cortex development. Development (Cambridge, England) 135 10821753
2007 MOZ and MORF, two large MYSTic HATs in normal and cancer stem cells. Oncogene 119 17694082
2012 Mutations in KAT6B, encoding a histone acetyltransferase, cause Genitopatellar syndrome. American journal of human genetics 113 22265014
2015 MOZ and MORF acetyltransferases: Molecular interaction, animal development and human disease. Biochimica et biophysica acta 107 25920810
2006 The transcriptional coactivator Querkopf controls adult neurogenesis. The Journal of neuroscience : the official journal of the Society for Neuroscience 105 17079664
2011 Disruption of the histone acetyltransferase MYST4 leads to a Noonan syndrome-like phenotype and hyperactivated MAPK signaling in humans and mice. The Journal of clinical investigation 96 21804188
2019 Histone H3K23-specific acetylation by MORF is coupled to H3K14 acylation. Nature communications 90 31624313
2012 De novo mutations of the gene encoding the histone acetyltransferase KAT6B cause Genitopatellar syndrome. American journal of human genetics 86 22265017
2020 The key roles of the lysine acetyltransferases KAT6A and KAT6B in physiology and pathology. Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy 82 33130515
2004 Uterine leiomyomata with t(10;17) disrupt the histone acetyltransferase MORF. Cancer research 81 15313893
2012 Tandem PHD fingers of MORF/MOZ acetyltransferases display selectivity for acetylated histone H3 and are required for the association with chromatin. Journal of molecular biology 77 23063713
2015 KAT6B Is a Tumor Suppressor Histone H3 Lysine 23 Acetyltransferase Undergoing Genomic Loss in Small Cell Lung Cancer. Cancer research 73 26208904
2012 The KAT6B-related disorders genitopatellar syndrome and Ohdo/SBBYS syndrome have distinct clinical features reflecting distinct molecular mechanisms. Human mutation 70 22715153
2016 Decreased MORF leads to prolonged endoplasmic reticulum stress in periodontitis-associated chronic inflammation. Cell death and differentiation 62 27447113
2020 Brainwide Genetic Sparse Cell Labeling to Illuminate the Morphology of Neurons and Glia with Cre-Dependent MORF Mice. Neuron 58 32795398
2014 Further delineation of the KAT6B molecular and phenotypic spectrum. European journal of human genetics : EJHG 57 25424711
2011 Recognition of unmodified histone H3 by the first PHD finger of bromodomain-PHD finger protein 2 provides insights into the regulation of histone acetyltransferases monocytic leukemic zinc-finger protein (MOZ) and MOZ-related factor (MORF). The Journal of biological chemistry 57 21880731
2018 OPAL: prediction of MoRF regions in intrinsically disordered protein sequences. Bioinformatics (Oxford, England) 56 29360926
2017 The conserved domain in MORF proteins has distinct affinities to the PPR and E elements in PPR RNA editing factors. Biochimica et biophysica acta. Gene regulatory mechanisms 49 28549935
2017 Recognition of Histone H3K14 Acylation by MORF. Structure (London, England : 1993) 48 28286003
2020 Further delineation of the clinical spectrum of KAT6B disorders and allelic series of pathogenic variants. Genetics in medicine : official journal of the American College of Medical Genetics 47 32424177
2018 miR-22/KAT6B axis is a chemotherapeutic determiner via regulation of PI3k-Akt-NF-kB pathway in tongue squamous cell carcinoma. Journal of experimental & clinical cancer research : CR 46 30041677
2013 De novo mutations of the gene encoding the histone acetyltransferase KAT6B in two patients with Say-Barber/Biesecker/Young-Simpson syndrome. American journal of medical genetics. Part A 38 23436491
2012 Querkopf is a key marker of self-renewal and multipotency of adult neural stem cells. Journal of cell science 36 22331353
2014 An individual with blepharophimosis-ptosis-epicanthus inversus syndrome (BPES) and additional features expands the phenotype associated with mutations in KAT6B. American journal of medical genetics. Part A 35 24458743
2015 Novel KAT6B-KANSL1 fusion gene identified by RNA sequencing in retroperitoneal leiomyoma with t(10;17)(q22;q21). PloS one 34 25621995
2018 OPAL+: Length-Specific MoRF Prediction in Intrinsically Disordered Protein Sequences. Proteomics 32 30324701
2019 Kat6b Modulates Oct4 and Nanog Binding to Chromatin in Embryonic Stem Cells and Is Required for Efficient Neural Differentiation. Journal of molecular biology 31 30790630
2012 Detection of Aspergillus fumigatus pulmonary fungal infections in mice with (99m)Tc-labeled MORF oligomers targeting ribosomal RNA. Nuclear medicine and biology 30 23142409
2022 Recurrent KAT6B/A::KANSL1 Fusions Characterize a Potentially Aggressive Uterine Sarcoma Morphologically Overlapping With Low-grade Endometrial Stromal Sarcoma. The American journal of surgical pathology 29 35575789
2022 BRPF1-KAT6A/KAT6B Complex: Molecular Structure, Biological Function and Human Disease. Cancers 29 36077605
2015 A patient showing features of both SBBYSS and GPS supports the concept of a KAT6B-related disease spectrum, with mutations in mid-exon 18 possibly leading to combined phenotypes. European journal of medical genetics 29 26370006
2013 Epigenetic influence of KAT6B and HDAC4 in the development of skeletal malocclusion. American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics 29 24075665
2010 Emerging role of the MORF/MRG gene family in various biological processes, including aging. Annals of the New York Academy of Sciences 29 20536842
2017 Bivalent complexes of PRC1 with orthologs of BRD4 and MOZ/MORF target developmental genes in Drosophila. Genes & development 27 29070704
2015 MORF-RELATED GENE702, a Reader Protein of Trimethylated Histone H3 Lysine 4 and Histone H3 Lysine 36, Is Involved in Brassinosteroid-Regulated Growth and Flowering Time Control in Rice. Plant physiology 27 25855537
2013 KAT5 and KAT6B are in positive regulation on cell proliferation of prostate cancer through PI3K-AKT signaling. International journal of clinical and experimental pathology 27 24294372
2003 A novel fusion variant of the MORF and CBP genes detected in therapy-related myelodysplastic syndrome with t(10;16)(q22;p13). British journal of haematology 27 12542485
2007 The role of the MORF/MRG family of genes in cell growth, differentiation, DNA repair, and thereby aging. Annals of the New York Academy of Sciences 26 17460191
2020 Aging-associated decrease in the histone acetyltransferase KAT6B is linked to altered hematopoietic stem cell differentiation. Experimental hematology 24 32014431
2019 MicroRNA-4513 Promotes Gastric Cancer Cell Proliferation and Epithelial-Mesenchymal Transition Through Targeting KAT6B. Human gene therapy. Clinical development 24 31310159
2007 Investigation of MYST4 histone acetyltransferase and its involvement in mammalian gametogenesis. BMC developmental biology 24 17980037
2023 MORF and MOZ acetyltransferases target unmethylated CpG islands through the winged helix domain. Nature communications 23 36754959
2023 The KAT6B::KANSL1 Fusion Defines a New Uterine Sarcoma With Hybrid Endometrial Stromal Tumor and Smooth Muscle Tumor Features. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 23 37307879
2007 Cell studies of a three-component antisense MORF/tat/Herceptin nanoparticle designed for improved tumor delivery. Cancer gene therapy 20 18084241
2004 Variant MYST4-CBP gene fusion in a t(10;16) acute myeloid leukaemia. British journal of haematology 20 15147375
2014 Molecular motor MYO1C, acetyltransferase KAT6B and osteogenetic transcription factor RUNX2 expression in human masseter muscle contributes to development of malocclusion. Archives of oral biology 19 24698832
2013 (99m)Tc-MORF oligomers specific for bacterial ribosomal RNA as potential specific infection imaging agents. Bioorganic & medicinal chemistry 18 24054488
2024 Increasing histone acetylation improves sociability and restores learning and memory in KAT6B-haploinsufficient mice. The Journal of clinical investigation 17 38557491
2020 CircKIAA0907 Retards Cell Growth, Cell Cycle, and Autophagy of Gastric Cancer In Vitro and Inhibits Tumorigenesis In Vivo via the miR-452-5p/KAT6B Axis. Medical science monitor : international medical journal of experimental and clinical research 16 32722658
2019 Leiomyoma with KAT6B-KANSL1 fusion: case report of a rapidly enlarging uterine mass in a postmenopausal woman. Diagnostic pathology 16 31027501
2015 A recurrent synonymous KAT6B mutation causes Say-Barber-Biesecker/Young-Simpson syndrome by inducing aberrant splicing. American journal of medical genetics. Part A 16 26334766
2003 Expression, purification, and analysis of MOZ and MORF histone acetyltransferases. Methods (San Diego, Calif.) 16 12893170
2018 The Kat in the HAT: The Histone Acetyl Transferase Kat6b (MYST4) Is Downregulated in Murine Macrophages in Response to LPS. Mediators of inflammation 15 29977151
2017 Lin-Gettig syndrome: Craniosynostosis expands the spectrum of the KAT6B related disorders. American journal of medical genetics. Part A 15 28696035
2004 Querkopf, a histone acetyltransferase, is essential for embryonic neurogenesis. Frontiers in bioscience : a journal and virtual library 15 14766340
2023 Circ-MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR-506-3p/KAT6B axis. The Kaohsiung journal of medical sciences 14 37272875
2008 Synthesis and in vitro characterization of a dendrimer-MORF conjugate for amplification pretargeting. Bioconjugate chemistry 14 18646837
2024 The histone acetyltransferase KAT6B is required for hematopoietic stem cell development and function. Stem cell reports 13 38518784
2017 A Say-Barber-Biesecker-Young-Simpson variant of Ohdo syndrome with a KAT6B 10-base pair palindromic duplication: A recurrent mutation causing a severe phenotype mixed with genitopatellar syndrome. Congenital anomalies 13 27696664
2011 Human islet cell MORF/cMORF pretargeting in a xenogeneic murine transplant model. Molecular pharmaceutics 13 21361360
2010 Affinity enhancement pretargeting: synthesis and testing of a 99mTc-labeled bivalent MORF. Molecular pharmaceutics 13 20507096
2021 Novel variants in KAT6B spectrum of disorders expand our knowledge of clinical manifestations and molecular mechanisms. Molecular genetics & genomic medicine 12 34519438
2017 A novel truncating variant within exon 7 of KAT6B associated with features of both Say-Barber-Bieseker-Young-Simpson syndrome and genitopatellar syndrome: Further evidence of a continuum in the clinical spectrum of KAT6B-related disorders. American journal of medical genetics. Part A 12 29226580
2024 Superenhancer-driven circRNA Myst4 involves in pulmonary artery smooth muscle cell ferroptosis in pulmonary hypertension. iScience 11 39351203
2024 Uterine mesenchymal tumours harboring the KAT6B/A::KANSL1 gene fusion represent a distinct type of uterine sarcoma based on DNA methylation profiles. Virchows Archiv : an international journal of pathology 11 39392508
2022 circUBAP2 inhibits cisplatin resistance in gastric cancer via miR-300/KAT6B axis. Anti-cancer drugs 11 36206113
2017 Identifying the KAT6B Mutation via Diagnostic Exome Sequencing to Diagnose Say-Barber-Biesecker-Young-Simpson Syndrome in Three Generations of a Family. Annals of rehabilitation medicine 11 28758091
2022 KAT6B May Be Applied as a Potential Therapeutic Target for Glioma. Journal of oncology 10 35432536
2023 Downregulation of ciRNA-Kat6b in dorsal spinal horn is required for neuropathic pain by regulating Kcnk1 in miRNA-26a-dependent manner. CNS neuroscience & therapeutics 9 37144575
2017 De Novo Mutation of KAT6B Gene Causing Atypical Say-Barber-Biesecker-Young-Simpson Syndrome or Genitopatellar Syndrome. Fetal and pediatric pathology 9 28426343
2007 Optical pretargeting of tumor with fluorescent MORF oligomers. Molecular imaging and biology 9 17171474
2025 KAT6B overexpression rescues embryonic lethality in homozygous null KAT6A mice restoring vitality and normal lifespan. Nature communications 8 40000651
2022 MoRF-FUNCpred: Molecular Recognition Feature Function Prediction Based on Multi-Label Learning and Ensemble Learning. Frontiers in pharmacology 8 35350759
2020 KAT6B Genetic Variant Identified in a Short Stature Chinese Infant: A Report of Physical Growth in Clinical Spectrum of KAT6B-Related Disorders. Frontiers in pediatrics 7 32391291
2009 In vivo delivery of antisense MORF oligomer by MORF/carrier streptavidin nanoparticles. Cancer biotherapy & radiopharmaceuticals 7 19877887
2023 DNA methylation episignatures are sensitive and specific biomarkers for detection of patients with KAT6A/KAT6B variants. Epigenomics 6 37249002
2016 De novo KAT6B Mutation Identified with Whole-Exome Sequencing in a Girl with Say-Barber/Biesecker/Young-Simpson Syndrome. Molecular syndromology 6 28232779
2024 The winged helix domain of MORF binds CpG islands and the TAZ2 domain of p300. iScience 5 38500836
2024 Uterine sarcoma with KAT6B/A::KANSL1 fusion: a molecular and clinicopathological study on 9 cases. Virchows Archiv : an international journal of pathology 5 39627614
2023 XBP1-elicited environment by chemotherapy potentiates repopulation of tongue cancer cells by enhancing miR-22/lncRNA/KAT6B-dependent NF-κB signalling. Clinical and translational medicine 5 36639835
2023 Clinical heterogeneity of polish patients with KAT6B-related disorder. Molecular genetics & genomic medicine 5 37658610
2022 Circular RNA circMRPS35 regulates progression and autophagy in osteosarcoma cells by recruiting KAT6B to govern FOXO3. Anti-cancer drugs 5 35503036
2024 ERα status of invasive ductal breast carcinoma as a result of regulatory interactions between lysine deacetylases KAT6A and KAT6B. Scientific reports 4 39505971
2023 Clinical features and underlying mechanisms of KAT6B disease in a Chinese boy. Molecular genetics & genomic medicine 4 37288707
2024 De novo KAT6B mutation causes Say-Barber-Biesecker-Young-Simpson variant of Ohdo syndrome in an Iranian boy: a case report. Journal of medical case reports 3 38178270
2024 MoRF_ESM: Prediction of MoRFs in disordered proteins based on a deep transformer protein language model. Journal of bioinformatics and computational biology 3 38812466
2019 Genitopatellar Syndrome Secondary to De Novo KAT6B Mutation: The First Genetically Confirmed Case in South Korea. Yonsei medical journal 3 30900427
2016 Features of KAT6B-related disorders in a patient with 10q22.1q22.3 deletion. Ophthalmic genetics 3 27880066
2025 Loss of KAT6B causes premature ossification and promotes osteoblast differentiation during development. Developmental biology 2 39832706
2025 KAT6B overexpression in mice causes aggression, anxiety, and epilepsy. iScience 2 40083716
2025 MORF proteins: A small family regulating organellar RNA editing and beyond. Journal of integrative plant biology 2 40662513
2023 A ribonuclease activity linked to DYW1 in vitro is inhibited by RIP/MORF proteins. Scientific reports 2 37400527
2017 [KAT6B promotes LPS-triggered IL-6 production via enhancing recruitment of H3K23 acetylation to IL-6 promoter region]. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 2 29268844
2024 Comprehensive identification, characterization, and expression analysis of the MORF gene family in Brassica napus. BMC plant biology 1 38816808

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