Affinage

HDAC3

Histone deacetylase 3 · UniProt O15379

Length
428 aa
Mass
48.8 kDa
Annotated
2026-06-10
100 papers in source corpus 48 papers cited in narrative 48 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HDAC3 is a nuclear class I histone deacetylase that orchestrates transcription, genome stability, and metabolic homeostasis by removing acetyl marks from both histones and a broad set of non-histone substrates (PMID:9501169, PMID:21075309). Its catalytic activity is held in check until it docks onto the NCoR1/SMRT (NCOR2) corepressors, an allosteric switch tuned by competing small-molecule ligands: inositol phosphates such as Ins(1,4,5,6)P4 promote HDAC3–NCoR complex assembly and activation, microbiota-derived InsP3 acts as an activating metabolite, while NADPH binds the same domains with higher affinity to disrupt the complex and dampen deacetylation (PMID:32731255, PMID:33462516). Through this corepressor axis HDAC3 deacetylates histone H3K9/H4K5/H4K12 to compact chromatin and enable double-strand break repair and DNA replication, and it sets up bivalent H3K9me3/H3K14ac chromatin with SETDB1/KAP1 (PMID:21075309, PMID:31097476, PMID:31858687). A defining feature is its functional dichotomy: HDAC3 can act either as an enzyme or as a catalytically dispensable scaffold, with catalytic-dead knock-in models showing that hepatic lipid metabolism (with NCOR1), spermatogenesis (via SOX30 recruitment), and macrophage inflammatory gene activation (at ATF2 sites) proceed without deacetylase activity, whereas skeletal muscle fuel metabolism requires it (PMID:24268577, PMID:32760002, PMID:33939832, PMID:30428023). HDAC3 is recruited to specific loci by sequence-specific factors—Rev-erbα/NCoR to drive circadian hepatic lipogenesis, BCL6/SMRT to repress immune enhancers, HOXB13 to suppress lipogenic genes, and TAL1/GATA2/ETS to build a flow-responsive enhanceosome (PMID:21900149, PMID:27733359, PMID:35468964, PMID:29035278). Beyond chromatin, HDAC3 deacetylates non-histone targets including p53 (suppressing apoptosis), NICD1, Msh3/MutSβ (activating trinucleotide repeat expansion), PML-RARα, FOXO1, Nrf2, SRF, and NF-κB p65, coupling it to apoptosis, mismatch-repair-driven instability, oncoprotein stability, and oxidative/inflammatory signaling (PMID:25305081, PMID:32107550, PMID:32900932, PMID:36894687, PMID:33454009). Its activity is further controlled by phosphorylation—PINK1, CK2α, and c-Src phosphorylate HDAC3 (S424, Y325/328/331) to enhance activity, PP4 dephosphorylation inactivates it—and by ubiquitin-dependent stability control via Mdm2, PDCD5/Siah2, and PIWIL2 (PMID:25305081, PMID:31430896, PMID:31268609, PMID:31358320, PMID:29555935, PMID:37345556).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1998 High

    Establishing that HDAC3 is a bona fide enzyme answered whether the gene encodes an active histone deacetylase rather than merely a homolog.

    Evidence Immunoprecipitation and in vitro deacetylase assays on free histones and nucleosomes with pharmacological inhibition

    PMID:9501169

    Open questions at the time
    • Did not define physiological substrates or cofactor requirements
    • Genomic targeting and regulation unaddressed
  2. 2006 Medium

    Linking laminar flow signaling to HDAC3 activation showed it transduces mechanical/growth signals into deacetylation of p53 to drive endothelial differentiation.

    Evidence ES cell differentiation under laminar flow with kinase inhibitors, HDAC3 KD/OE, and p53 deacetylation assay

    PMID:16982804

    Open questions at the time
    • Single lab; direct vs indirect p53 deacetylation not fully separated
    • Upstream PI3K/Akt to HDAC3 connection inferred via inhibitors
  3. 2010 High

    Defining the HDAC3/NCoR/SMRT axis as required for chromatin integrity established its role in DNA replication and genome stability beyond transcription.

    Evidence Liver-specific Hdac3 KO and NCOR1/SMRT siRNA with histone-mark ChIP and DNA damage assays

    PMID:21075309

    Open questions at the time
    • Whether genomic instability is direct or secondary to metabolic stress not resolved
    • Specific repair step not pinpointed
  4. 2011 High

    Mapping a circadian HDAC3 cistrome overlapping Rev-erbα/NCoR connected the clock machinery to rhythmic hepatic lipogenesis via epigenomic remodeling.

    Evidence Liver-specific KO with genome-wide ChIP-seq for HDAC3, NCoR, Rev-erbα, H3ac, and Pol II

    PMID:21900149

    Open questions at the time
    • Correlative cistrome overlap; causal recruitment hierarchy partly inferred
    • Catalytic vs scaffolding contribution not separated
  5. 2013 High

    Catalytic-dead rescue in liver revealed a deacetylase-independent function, fundamentally reframing HDAC3 as a dual enzyme/scaffold and distinguishing NCOR from SMRT requirement.

    Evidence Liver-specific KO, deacetylase-dead knock-in rescue, and NCOR/SMRT conditional KO with expression profiling

    PMID:24268577

    Open questions at the time
    • Molecular basis of scaffolding activity unresolved
    • Tissue-specificity of catalytic dependence not yet generalized
  6. 2015 High

    Identifying phosphorylation control (PINK1 S424; insulin/mTOR S424; c-Src and CK2α) and substrate switching established HDAC3 activity as signal-regulated and showed it tunes both p53/apoptosis and glycolytic PGK1.

    Evidence In vitro kinase/phosphatase assays, phospho-mimetic/deficient mutants, KO MEFs, and substrate deacetylation assays

    PMID:25305081 PMID:26077467 PMID:26356530

    Open questions at the time
    • Crosstalk between distinct phospho-sites not integrated
    • Stoichiometry of phosphorylation in vivo unknown
  7. 2016 High

    Defining the BCL6/SMRT/HDAC3 repressor at immune enhancers explained how CREBBP loss enables unopposed deacetylation and identified HDAC3 as a therapeutic vulnerability in lymphoma.

    Evidence ChIP-seq, reciprocal Co-IP of the complex, and conditional HDAC3 KO rescue in a murine lymphoma model

    PMID:27733359

    Open questions at the time
    • Generalizability across lymphoma subtypes not established
    • Direct vs enhancer-context-dependent recruitment not dissected
  8. 2018 High

    Tyrosine phosphorylation by c-Src at the C-terminus and Mdm2/PIWIL2-mediated stabilization defined post-translational control of HDAC3 activity and abundance in cancer contexts.

    Evidence In vitro kinase assays, domain-mapping Co-IP, phospho-deficient mutants, and ubiquitination/competitive binding assays

    PMID:29555935 PMID:30317579 PMID:31358320 PMID:31430896

    Open questions at the time
    • Several stability findings are single-lab Medium-confidence
    • Interplay of monoubiquitination vs degradative ubiquitination unclear
  9. 2019 High

    Comparative catalytic-dead knock-ins across tissues sharpened the enzyme-vs-scaffold dichotomy, showing muscle metabolism needs catalysis while spermatogenesis does not, and that SOX30 dictates testicular HDAC3 recruitment.

    Evidence NCoR/SMRT DAD-mutant knock-in mice, multiple tissue-specific KOs, ChIP-seq, and SOX30 epistasis

    PMID:30428023 PMID:31097476 PMID:31858687 PMID:33939832

    Open questions at the time
    • Mechanism distinguishing catalytic-dependent vs -independent loci unknown
    • How SOX30 and other TFs select scaffolding mode unresolved
  10. 2020 High

    Discovery of allosteric ligand control (InsP3 activation, NADPH inhibition competing for the Ins(1,4,5,6)P4 site) and non-canonical, NCoR-independent recruitment at ATF2 sites unified metabolic and inflammatory regulation of HDAC3.

    Evidence Direct biochemical activity/binding and competition assays, germ-free models, catalytic-dead knock-in, and ChIP-seq co-occupancy with ATF2/ATF3

    PMID:32731255 PMID:32760002 PMID:33462516

    Open questions at the time
    • Structural basis of ligand competition not solved
    • How metabolite levels are sensed at specific loci in vivo unclear
  11. 2020 High

    Expanding the non-histone substrate set (NICD1, Msh3/MutSβ, ELL) and target genes (CXCL9/10/11) connected HDAC3 to Notch signaling, trinucleotide repeat instability, transcription elongation, and antitumor immunity.

    Evidence Genetic KO, site-specific acetylation mutants, stability and ubiquitination assays, ChIP, and immunocompetent tumor models

    PMID:32107550 PMID:32152128 PMID:32900932 PMID:36898011

    Open questions at the time
    • Direct vs indirect deacetylation for some substrates relies on single studies
    • In vivo substrate hierarchy not ranked
  12. 2023 High

    Mapping locus-specific recruitment partners (HOXB13, KLF5, p65/NF-κB) and additional non-histone substrates (PML-RARα, FOXO1, Nrf2, SRF) extended HDAC3 across lipogenesis, ferroptosis, fibrosis, and oxidative/inflammatory disease.

    Evidence Co-IP, site-specific acetylation mutants, ChIP at target promoters/enhancers, and in vivo disease/xenograft models

    PMID:35468964 PMID:36894687 PMID:37244125 PMID:37890360 PMID:38322347 PMID:39505146

    Open questions at the time
    • Many disease links are single-lab Medium-confidence
    • Whether scaffolding or catalysis dominates each context not uniformly tested
  13. 2024 Medium

    Identification of HDAC3 delactylase activity and reciprocal H4K12-lactylation feedback positioned HDAC3 at the interface of lactate metabolism and chromatin in senescence and inflammation.

    Evidence KO mouse models, ChIP/CUT&Tag for H4K12la at SASP and TGF-β promoters, and HDAC3 delactylase activity assays

    PMID:39088352 PMID:39945346

    Open questions at the time
    • Single-lab Medium-confidence; direct delactylase catalysis vs indirect effects needs reconstitution
    • Generality of lactylation substrate across loci unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • The structural and molecular rule that determines when HDAC3 functions as an enzyme versus a catalytically dispensable scaffold at a given locus remains undefined.
  • No structural model explaining ligand-gated catalytic/scaffold switching
  • Unclear how transcription factors select recruitment mode
  • Substrate selection rules among competing non-histone targets unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 6 GO:0140110 transcription regulator activity 5 GO:0016787 hydrolase activity 3 GO:0042393 histone binding 3 GO:0098772 molecular function regulator activity 2
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 3 GO:0005886 plasma membrane 1
Pathway
R-HSA-74160 Gene expression (Transcription) 6 R-HSA-1430728 Metabolism 5 R-HSA-168256 Immune System 5 R-HSA-4839726 Chromatin organization 5 R-HSA-73894 DNA Repair 3 R-HSA-5357801 Programmed Cell Death 2 R-HSA-9909396 Circadian clock 1
Partners
BCL6HOXB13MDM2NCOR1NCOR2PDCD5PIWIL2SOX30
Complex memberships
BCL6/SMRT/HDAC3 repressor complexHDAC3-NCoR1/SMRT corepressor complexSETDB1/KAP1/HDAC3 complexTAL1/GATA2/ETS1-2/HDAC3/EP300 enhanceosome

Evidence

Reading pass · 48 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 HDAC3 encodes a 428-amino acid nuclear protein that exhibits histone deacetylase activity on both free histones and purified nucleosomes; activity is inhibited by trichostatin A, trapoxin, and butyrate in vitro, establishing it as a human RPD3 ortholog with enzymatic deacetylase function. Immunoprecipitation, in vitro deacetylase assay on free histones and nucleosomes, pharmacological inhibition, Western blot/subcellular fractionation Proceedings of the National Academy of Sciences of the United States of America High 9501169
2010 HDAC3 is required for efficient DNA replication and DNA damage repair; loss of HDAC3 increases H3K9/K14ac, H4K5ac, and H4K12ac, impairs chromatin compaction and heterochromatin content, and retains histone deposition marks. siRNA targeting of the HDAC3 cofactors NCOR1 and SMRT (NCOR2) increases H4K5ac and causes DNA damage, establishing the HDAC3/NCOR/SMRT axis as critical for chromatin structure and genomic stability. Conditional liver-specific Hdac3 knockout, siRNA knockdown of NCOR1/SMRT, ChIP for histone modifications, DNA damage assays Cancer cell High 21075309
2013 Deacetylase-dead HDAC3 mutants rescue hepatosteatosis and repress lipogenic gene expression in HDAC3-depleted mouse liver, demonstrating a deacetylase-independent transcriptional function. Interaction with NCOR (but not SMRT) is essential for this in vivo function; liver-specific NCOR knockout phenocopies HDAC3 loss metabolically. Liver-specific knockout, knock-in of deacetylase-dead mutants, pharmacologic HDAC inhibition in primary hepatocytes, liver-specific NCOR/SMRT knockouts, gene expression analysis Molecular cell High 24268577
2011 HDAC3 genomic occupancy in mouse liver follows a pronounced circadian pattern on lipid metabolism genes, inversely correlating with histone acetylation and RNA polymerase II recruitment. The HDAC3 cistrome overlaps significantly with Rev-erbα and its binding partner NCoR, linking circadian clock machinery to hepatic de novo lipogenesis via HDAC3-mediated epigenomic remodeling. Liver-specific Hdac3 knockout, genome-wide ChIP-seq for HDAC3, NCoR, Rev-erbα, H3 acetylation, and RNA Pol II Cold Spring Harbor symposia on quantitative biology High 21900149
2006 Laminar flow stabilizes and activates HDAC3 through the Flk-1–PI3K–Akt pathway; activated HDAC3 deacetylates p53, leading to p21 activation and endothelial progenitor cell differentiation into endothelial cells. ES cell differentiation assay under laminar flow/VEGF, kinase pathway inhibitors, HDAC3 knockdown/overexpression, p53 deacetylation assay The Journal of cell biology Medium 16982804
2015 PGK1 is acetylated at lysine 220 (inhibiting its activity) by KAT9, and deacetylated by HDAC3. Insulin activates the PI3K/AKT/mTOR pathway to phosphorylate HDAC3 at S424, promoting HDAC3–PGK1 interaction and K220 deacetylation, thereby stimulating PGK1 enzymatic activity. Co-IP, in vitro deacetylation assay, acetylation-mimetic/deficient mutants, mTOR pathway inhibitors, phospho-specific analysis PLoS biology High 26356530
2020 During LPS-stimulated macrophage activation, HDAC3 is recruited to ATF2-bound chromatin sites without NCoR1/2 and activates inflammatory gene expression through a non-canonical, deacetylase-independent mechanism. Conversely, HDAC3 deacetylase activity is selectively engaged at ATF3-bound sites to suppress Toll-like receptor signaling. Loss of HDAC3 protects mice from lethal LPS exposure, but abolition of catalytic activity alone does not confer this protection. Macrophage-specific Hdac3 knockout, catalytic-dead HDAC3 knock-in, ChIP-seq, genomic co-occupancy analysis with ATF2/ATF3, in vivo LPS challenge Nature High 32760002
2020 Microbiota-derived inositol-1,4,5-trisphosphate (InsP3) directly promotes HDAC3 activity in intestinal epithelial cells, activating HDAC3-dependent proliferation and counteracting butyrate inhibition. InsP3 and Ins(1,4,5,6)P4 bind the same domains on HDAC3; while Ins(1,4,5,6)P4 promotes HDAC3–NCoR complex formation, InsP3 acts as an activating metabolite. Germ-free vs microbiota-replete mouse comparison, intestinal organoids, biochemical HDAC3 activity assay, InsP3/phytate treatment, HDAC3 knockout cells Nature High 32731255
2021 NADPH directly binds HDAC3 and disrupts the association between HDAC3 and its co-activators NCoR2 (SMRT) or NCoR1, impairing HDAC3 activation and thereby increasing histone acetylation. NADPH and Ins(1,4,5,6)P4 compete for the same binding domains on HDAC3, with NADPH having higher affinity, whereas Ins(1,4,5,6)P4 promotes HDAC3–NCoR complex formation. NADPH binding assay, Co-IP of HDAC3–NCoR disruption, competitive binding with Ins(1,4,5,6)P4, HDAC3 inhibitor rescue, knockdown of NADPH-generating enzymes Nature metabolism High 33462516
2016 BCL6 forms a repressor complex with SMRT and HDAC3 that binds extensively to MHC class II loci and other enhancers; CREBBP loss enables unopposed deacetylation at these enhancers by BCL6/SMRT/HDAC3, silencing B-cell signaling and immune response genes. HDAC3 loss-of-function rescues enhancer H3K27 acetylation and gene expression, suppressing CREBBP-mutant lymphomas. ChIP-seq, Co-IP of BCL6/SMRT/HDAC3 complex, conditional HDAC3 KO in murine lymphoma model, in vitro and in vivo rescue experiments Cancer discovery High 27733359
2015 HDAC3 deacetylates p53 and suppresses p53-dependent apoptosis. PINK1 phosphorylates HDAC3 at Ser-424, enhancing its deacetylase activity and promoting direct association with p53, leading to p53 hypoacetylation. Protein phosphatase 4c reverses PINK1-mediated HDAC3 phosphorylation. PINK1-mediated phosphorylation also prevents oxidative stress-induced C-terminal cleavage of HDAC3. Co-IP, in vitro kinase assay (PINK1 phosphorylating HDAC3), phospho-mimetic mutant HDAC3(S424E), PINK1 KO MEFs, deacetylase activity assay, phosphatase assay Human molecular genetics High 25305081
2015 PDCD5 mediates dissociation of HDAC3 from p53 under genotoxic stress, leading to HDAC3 cleavage and ubiquitin-dependent proteasomal degradation; this releases p53 inhibition. Casein kinase 2α phosphorylates PDCD5 at Ser-119 to stabilize it and promote importin 13-mediated nuclear translocation of PDCD5. PDCD5 deletion abrogates etoposide-induced p53 stabilization and HDAC3 cleavage. Co-IP, ubiquitination assay, PDCD5 KO MEFs, CK2α kinase assay, importin 13 interaction assay, proteasome inhibitor experiments Nature communications High 26077467
2019 HDAC3 deacetylates H3K9 specifically; ablation of HDAC3 (but not other class I HDACs) disrupts H3K9 deacetylation and the consequent trimethylation of H3K9 (H3K9me3), impairing the first step of double-strand break repair. Hyperacetylated H3K9ac simultaneously acts as a transcriptional activator, promoting tumorigenic signaling. Individual class I HDAC KO mouse models, ChIP for H3K9ac/H3K9me3, DNA damage assays, gene expression analysis Cancer research High 31097476
2017 In response to oscillatory shear stress, transcription factors TAL1, GATA2, and ETS1/2 physically interact with and recruit HDAC3 to the E-box–GATA–ETS composite element of a GATA2 intragenic enhancer. HDAC3 in turn recruits histone acetyltransferase EP300 to form an enhanceosome complex that promotes GATA2 expression, which is required for lymphovenous and lymphatic valve morphogenesis. Endothelium-specific Hdac3 KO in mice, Co-IP of HDAC3 with TAL1/GATA2/ETS1/2/EP300, ChIP at GATA2 enhancer, shear stress assay The Journal of clinical investigation High 29035278
2019 HDAC3 controls the meiotic-to-postmeiotic transition in spermatogenesis in a deacetylase-independent manner. Abolishing HDAC3 catalytic activity via NCoR/SMRT knock-in mutations causes histone hyperacetylation identical to KO but does not cause infertility, whereas KO does. SOX30 recruits HDAC3 to its genomic binding sites in testes; loss of SOX30 abolishes HDAC3 cistromic recruitment. Three independent testis-specific Hdac3 KO mouse lines, NCoR/SMRT catalytic-dead knock-in mice, RNA-seq, histone acetylation ChIP-seq, SOX30 KO Nucleic acids research High 33939832
2019 HDAC3 enzymatic activity is required for skeletal muscle fuel metabolism. NS-DADm knock-in mice (which ablate HDAC3 deacetylase activity via NCoR/SMRT mutations without altering HDAC3 protein levels) show the same metabolic phenotypes as HDAC3-depleted muscle—reduced force generation, enhanced fatty acid oxidation, reduced glucose uptake, altered BCAA catabolism gene expression—establishing that, unlike in liver or embryonic development, the muscle metabolic function requires catalytic activity. NCoR/SMRT DAD-mutant knock-in mouse model (NS-DADm), metabolic phenotyping, gene expression analysis, comparison to muscle-specific HDAC3 KO Journal of molecular cell biology High 30428023
2019 PP4-dependent dephosphorylation of HDAC3 inactivates its catalytic activity following peripheral nerve injury, enhancing histone H3K9 acetylation and enabling a regenerative gene expression program. Central spinal cord injury does not trigger this calcium–PP4–HDAC3 dephosphorylation cascade, explaining regenerative failure. Genetic or pharmacological HDAC3 inhibition overcomes regenerative failure after spinal cord injury. Pharmacological screen in DRG neurons, in vivo PP4 inhibitor, H3K9ac ChIP-seq from ex vivo DRG, RNA-seq, genetic HDAC3 inhibition, spinal cord injury model The EMBO journal High 31268609
2020 HDAC3 controls NICD1 (Notch1 intracellular domain) acetylation levels, directly affecting NICD1 protein stability. Genetic loss-of-function of HDAC3 or nanomolar HDAC inhibitor treatment reduces Notch target gene expression with local reduction of histone acetylation. An HDAC3-insensitive NICD1 mutant is more stable but biologically less active. Hdac3 genetic KO, HDAC inhibitor treatment, NICD1 acetylation assay, NICD1 stability (cycloheximide chase), HDAC3-insensitive NICD1 mutant expression Nucleic acids research High 32107550
2020 HDAC3 deacetylates the MutSβ subunit Msh3 at five key lysine residues to activate MutSβ-driven trinucleotide repeat expansions. HDAC3 inhibition suppresses repeat expansion without impairing canonical mismatch repair; Msh3 arginine-substitution mutants at these lysine residues bypass the inhibitory effect of HDAC3 inhibitor. HDAC3 activity also partially controls MutSβ nuclear localization via deacetylation sites overlapping the Msh3 nuclear localization signal. HDAC3-selective inhibitor RGFP966, Msh3 lysine-to-arginine mutants, trinucleotide repeat expansion assay, mismatch repair assay, subcellular localization analysis Proceedings of the National Academy of Sciences of the United States of America High 32900932
2018 HDAC3 inhibition reduces SMARCA4 activity, derepressing miR-27a, which in turn destabilizes PAX3:FOXO1 mRNA in alveolar rhabdomyosarcoma cells. This HDAC3–SMARCA4–miR-27a–PAX3:FOXO1 circuit drives chemoresistance. HDAC3-selective inhibition (entinostat), HDAC3 genetic knockdown, miR-27a quantification, PAX3:FOXO1 mRNA stability assay, SMARCA4 activity assay, preclinical mouse models Science signaling Medium 30459282
2019 HDAC3 loss in the uterus causes implantation failure and decidualization defects through aberrant transcriptional activation of COL1A1 and COL1A2 genes; HDAC3 normally represses these collagen genes. Reduction of HDAC3 leads to p300 recruitment to Col1a1/Col1a2 loci; inhibition of p300 permits decidualization in HDAC3-attenuated cells. Conditional Hdac3 KO in PGR-positive cells (mouse uterus), expression microarray, ChIP-seq, primary human endometrial stromal cell culture, p300 inhibitor rescue Science translational medicine High 30626716
2019 HDAC3 occupies H3K9me3/H3K14ac bivalent chromatin regions in liver together with H3K9 methyltransferase SETDB1 in a KAP1 complex, correlating with H3K9me3 presence. This bivalent state is reduced with aging, and associated genes (regulating cholesterol secretion and triglyceride synthesis) are upregulated when bivalency is lost. Quantitative targeted mass spectrometry of histone modifications, sequential ChIP-seq (reChIP), bulk ChIP-seq for HDAC3/SETDB1/KAP1, young vs aged liver comparison Aging cell Medium 31858687
2018 c-Src kinase directly phosphorylates HDAC3 at tyrosine residues Y325, Y328, and Y331 (C-terminal domain), increasing HDAC3 deacetylase activity. EGF stimulation via EGFR activates c-Src to phosphorylate HDAC3, which is then recruited to the plasma membrane. Phosphorylation-deficient HDAC3(Y328/331A) lacks deacetylase activity and reduces breast cancer cell invasiveness. Co-IP, in vitro kinase assay (c-Src phosphorylating HDAC3), phospho-specific antibody, phospho-deficient mutant HDAC3, TIRF microscopy for membrane recruitment, invasion assay Cells High 31430896
2018 c-Src directly binds the C-terminal domain (277–428 aa) of HDAC3 and phosphorylates HDAC3 at Y325, Y328, and Y331; wild-type but not kinase-inactive c-Src (K298M) increases HDAC3 deacetylase activity. Triple alanine substitution of these tyrosines abolishes deacetylase activity. Phosphorylation-dependent HDAC3 activity promotes proliferation of HER2-positive breast cancer cells. Co-IP with deletion mutants, in vitro kinase assay, deacetylase activity assay, phospho-deficient triple mutant, proliferation assay Journal of cellular physiology High 30317579
2019 Mdm2 directly interacts with HDAC3 and induces HDAC3 monoubiquitination (requiring the Mdm2 RING domain), which stabilizes HDAC3 protein without altering its mRNA levels. MdmX cooperates with Mdm2 in this regulation. Mdm2 ablation decreases HDAC3 levels and reduces cell migration. Co-IP, ectopic expression of wild-type vs. RING-mutant Mdm2, ubiquitination assay, Mdm2 knockdown, migration assay Biochemical and biophysical research communications Medium 31358320
2018 PIWIL2 interacts with HDAC3, stabilizing it by competing with the E3 ubiquitin ligase Siah2 for binding, thereby preventing ubiquitin-mediated HDAC3 degradation. PIWIL2 also facilitates interaction between HDAC3 and CK2α, promoting CK2α-mediated phosphorylation and activation of HDAC3. Co-IP of PIWIL2/HDAC3/Siah2/CK2α, competitive binding assay, ubiquitination assay, HDAC3 activity assay Cell death & disease Medium 29555935
2020 PACS-1 interacts with HDAC2 and HDAC3 in the nucleus and is required for HDAC2/HDAC3-dependent chromatin maturation. PACS-1 knockdown causes proteasome-mediated degradation of HDAC2 and HDAC3, leading to elevated H3K9 and H4K16 acetylation and increased replication stress-induced DNA damage. Co-IP of PACS-1 with HDAC2/HDAC3, PACS-1 knockdown, proteasome inhibitor rescue, histone modification analysis, DNA damage assays Oncogene Medium 31988453
2020 DBC1 competes with HDAC3 for the same binding sites on the transcription elongation factor ELL, thereby preventing HDAC3-mediated deacetylation and consequent destabilization of ELL. HDAC3-mediated deacetylation of ELL promotes its polyubiquitylation by Siah1 E3 ligase, leading to ELL degradation; p300-mediated acetylation has the opposing stabilizing effect. Co-IP of DBC1/HDAC3/p300/Siah1 with ELL, competitive binding assay, acetylation/ubiquitination assays, DBC1 knockdown, gene expression analysis Proceedings of the National Academy of Sciences of the United States of America High 32152128
2022 HDAC3 deacetylase activity is required for FGF9 and IGF2 expression in epicardial cells to promote myocardial growth; Hdac3 KO epicardial cells upregulate miR-322 and miR-503, which repress FGF9 and IGF2. FGF9 or IGF2 supplementation rescues the myocardial proliferation defect. Knockdown of miR-322 or miR-503 restores FGF9/IGF2 expression in Hdac3 KO cells. Epicardial-specific Hdac3 KO mouse, transcriptomic analysis, miRNA quantification, miR-322/miR-503 overexpression/knockdown, FGF9/IGF2 rescue experiment Circulation research Medium 35722872
2017 HDAC3 inhibition triggers degradation of c-Myc protein, leading to downregulation of DNMT1 expression in multiple myeloma cells. Additionally, HDAC3 inhibition causes hyperacetylation of DNMT1 protein itself, reducing its stability. HDAC3 knockdown (but not HDAC1 or HDAC2) specifically mediates these effects. HDAC3-selective siRNA (vs HDAC1/HDAC2), HDAC3-selective inhibitor BG45, c-Myc degradation assay, DNMT1 acetylation and stability assay, xenograft mouse model Leukemia Medium 28490812
2023 HDAC3 deacetylates PML-RARα at lysine 394, reducing PIAS1-mediated SUMOylation and subsequent RNF4-induced ubiquitylation, thereby stabilizing the PML-RARα oncoprotein. HDAC3 inhibition promotes PML-RARα ubiquitylation and degradation in both wild-type and ATRA/ATO-resistant APL cells. Co-IP, in vitro deacetylation assay, acetylation mutant of PML-RARα at K394, SUMOylation and ubiquitylation assays, HDAC3 inhibitor/genetic KD, xenograft models Cell death and differentiation High 36894687
2022 HOXB13 physically interacts with HDAC3 (interaction disrupted by the G84E cancer-associated mutation) and recruits HDAC3 to lipogenic enhancers to catalyze histone deacetylation and suppress lipogenic regulators including FASN, independently of androgen receptor. Co-IP of HOXB13/HDAC3, ChIP-seq for HDAC3 and HOXB13 at lipogenic enhancers, HOXB13 G84E mutant interaction assay, HDAC3 histone deacetylation assay at enhancers, xenograft tumor metastasis model Nature genetics High 35468964
2023 HDAC3 directly binds to the Gpx4 promoter together with transcription factor KLF5 upon aristolochic acid treatment, causing local histone hypoacetylation and transcriptional inhibition of GPX4, which drives ferroptosis during AKI-CKD transition. HDAC3 and KLF5 co-IP confirms inducible association. HDAC3 conditional KO, HDAC3-selective inhibitor RGFP966, Co-IP of HDAC3/KLF5, ChIP at Gpx4 promoter, KLF5 inhibitor ML264, GPX4 inactivator RSL3 rescue experiment Redox biology Medium 37890360
2023 HDAC3 deacetylates FOXO1 and promotes its nuclear translocation in LPS-stimulated alveolar epithelial cells; nuclear FOXO1 transcriptionally activates ROCK1, which upon phosphorylation by RhoA disrupts mitochondrial quality control and promotes acute lung injury. HDAC3 conditional KO (Sftpc-cre; Hdac3f/f), FOXO1 acetylation assay, nuclear fractionation, ROCK1 promoter analysis, RhoA activation assay, pharmacological rescue Redox biology Medium 37244125
2023 HDAC3 interacts with and deacetylates Nrf2, reducing Nrf2 acetylation in cardiomyocytes. HDAC3 inhibition increases Nrf2 acetylation, while HDAC3 overexpression decreases it. Nrf2 acetylation promotes its activity and reduces oxidative stress. Co-IP of HDAC3/Nrf2, Nrf2 acetylation assay, HDAC3 inhibitor (RGFP966) vs adenoviral HDAC3 overexpression, Nrf2 inhibitor rescue Journal of advanced research Medium 39505146
2023 HDAC3 directly deacetylates SRF (serum response factor), enhancing SRF transcriptional activity in vascular smooth muscle cells; SMYD2 promotes HDAC3 expression via H3K36 tri-methylation at the HDAC3 promoter. HDAC3-SRF axis mediates VSMC phenotypic switching and neointimal hyperplasia in a deacetylase-dependent manner. Co-IP of HDAC3/SRF, SRF acetylation assay, SMYD2 ChIP at HDAC3 promoter, RGFP966 HDAC3 inhibitor, Smyd2-vTg and SMYD2 KD VSMCs, carotid artery injury model Acta pharmaceutica Sinica. B Medium 38322347
2023 Epithelial HDAC3 is essential for NF-κB-dependent regulation of epithelial MHC class II (MHCII) expression; epithelial MHCII reduces commensal-specific Th17 accumulation and protects against microbiota-triggered inflammation. Microbiota colonization concurrently induces epithelial HDAC3 expression and commensal-specific CD4+ T cells. Epithelium-specific Hdac3 KO, commensal-specific T cell tetramer analysis, ChIP for HDAC3 at MHCII locus, NF-κB pathway analysis, germ-free colonization experiments The Journal of clinical investigation High 36602872
2023 HDAC3 inhibition in liver reduces Hamp (hepcidin) mRNA via activation of the Hippo/YAP signaling pathway; HDAC3 loss leads to increased nuclear YAP translocation, and YAP binds repressor sites within the HAMP promoter to suppress hepcidin expression. Knock-in of constitutively active YAP (K342M) phenocopies hepcidin reduction in Hdac3-LKO mice. Hdac3 liver-specific KO, Hippo pathway inhibitor, YAP overexpression (constitutively active K342M knock-in), HAMP promoter reporter assay, Yap KD in Hdac3-LKO mice Research (Washington, D.C.) Medium 38034086
2023 PDCD5 promotes HDAC3 ubiquitination and degradation to reduce fibrotic responses; SMAD3 directly upregulates PDCD5 during cardiac fibrosis, and the resulting PDCD5-mediated HDAC3 inhibition suppresses profibrogenic gene expression. AAV9-mediated HDAC3 overexpression eliminates the protective effects of PDCD5 knock-in. Co-IP of PDCD5/HDAC3, HDAC3 ubiquitination assay, cardiac fibroblast KD/OE, fibroblast-specific PDCD5 knock-in mice, AAV9-HDAC3 rescue, SMAD3 ChIP Circulation research Medium 37345556
2024 TRAP1-mediated metabolic reprogramming increases aerobic glycolysis and lactate production, which down-regulates HDAC3 activity; reduced HDAC3 delactylase activity allows accumulation of H4K12 lactylation (H4K12la) at SASP promoters, activating SASP transcription and exacerbating VSMC senescence in atherosclerosis. VSMC-specific Trap1 KO mice, H4K12la ChIP at SASP promoters, HDAC3 activity assay (delactylase), metabolic profiling European heart journal Medium 39088352
2025 H4K12 lactylation (H4K12la) in macrophages inhibits HDAC3 expression, forming a feedback loop; HDAC3 activation reduces H4K12la levels. MCT1-mediated lactate uptake drives KAT5/KAT8-dependent H4K12la, which enriches at TGF-β1/TGF-β3 promoters and represses HDAC3. CUT&Tag and RNA-seq identified this feedback loop between H4K12la and HDAC3. CUT&Tag, RNA-seq, H4K12la ChIP at TGF-β promoters, HDAC3 overexpression rescue, macrophage depletion, MCT1 inhibitor Advanced science Medium 39945346
2020 HDAC3 transcriptionally promotes cGAS expression in microglia and potentiates cGAS-STING pathway activation by regulating acetylation and nuclear localization of p65 (NF-κB subunit). ChIP confirmed HDAC3 occupancy at the cGAS promoter region. Co-IP, ChIP, dual-luciferase reporter assay, microglial HDAC3 conditional KO, Western blot for p65 acetylation and localization Theranostics Medium 32863951
2020 HDAC3 directly binds to promoter regions of CXCL9, CXCL10, and CXCL11 to inhibit their expression; Hdac3-deficient tumor cells express high levels of these chemokines, recruiting CXCR3+ T cells to suppress tumor growth in immunocompetent mice. Hdac3 KO tumor cell lines, ChIP at CXCL9/10/11 promoters, CXCR3+ T cell infiltration quantification, immunocompetent vs immunodeficient mouse tumor models Cancer immunology research Medium 36898011
2020 Hdac3 microglial KO specifically inhibits proliferation of proinflammatory microglia after ischemic stroke by closing chromatin regions enriched with PU.1 motifs (ATAC-seq). AAV-mediated overexpression of PU.1 reverses HDAC3-KO-induced proliferation inhibition, establishing PU.1 as a downstream mediator of HDAC3 in stroke neuroinflammation. Microglial-specific Hdac3 KO, RNA-seq, ATAC-seq, AAV-PU.1 overexpression rescue, microglial proliferation assays Science advances High 38446877
2021 HDAC3 transactivates KDELR2 via CREB1; ChIP validated CREB1 binding to the KDELR2 promoter in an HDAC3-dependent manner. HDAC3-KDELR2 axis accelerates cell cycle progression by protecting centrosomal protein POC5 from proteasomal degradation. ChIP for CREB1 at KDELR2 promoter, HDAC3 KD, Co-IP of KDELR2/POC5, cell cycle analysis, breast cancer mouse model Cancer communications Medium 34146461
2018 PRDM16 physically interacts with HDAC3 in adipocytes; HDAC3-selective inhibitor RGFP966 induces thermogenic gene expression in murine and human fat cultures, but this induction is blunted in the absence of PRDM16, placing HDAC3 upstream of PRDM16 in the thermogenic program. Co-IP of PRDM16/HDAC3, HDAC3-selective inhibitor RGFP966 in murine and human fat cultures, PRDM16-null cells as epistasis control Endocrinology Medium 29757434
2015 Phosphorylation of HDAC3 at S424 (a mark necessary for deacetylase activity) is suppressed in osseous cells from aged mice, and HDAC3 expression is reduced in bone cells from postmenopausal compared to young women. Adenoviral restoration of Hdac3 in Hdac3-depleted bone marrow stromal cells restores normal gene expression, demonstrating direct causal control of glucocorticoid activation (Hsd11b1) and lipid storage (Fsp27/Cidec, Plin1) genes. Conditional Hdac3 KO in osteochondroprogenitors, adenoviral Hdac3 rescue, S424 phosphorylation analysis in aged vs young bone, gene expression profiling Journal of bone and mineral research Medium 26211746
2020 Hdac3 deacetylates the p65 subunit of NF-κB at K310, decreasing NF-κB DNA-binding and transcriptional activity in osteoclasts. Hdac3-deficient osteoclasts show increased K310 NF-κB acetylation, NF-κB hyperactivation, hypersensitivity to RANKL, and elevated bone resorption; Hdac3 also controls osteoclast-derived sphingosine-1-phosphate coupling to bone formation. Ctsk-cre conditional Hdac3 KO, NF-κB acetylation (K310) assay, RANKL responsiveness assay, pit formation (resorption) assay, sphingosine-1-phosphate production assay, conditioned medium mineralization assay The Journal of biological chemistry Medium 33454009

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 Hdac3 is essential for the maintenance of chromatin structure and genome stability. Cancer cell 299 21075309
2020 HDAC3 inhibition ameliorates ischemia/reperfusion-induced brain injury by regulating the microglial cGAS-STING pathway. Theranostics 279 32863951
1998 Characterization of a human RPD3 ortholog, HDAC3. Proceedings of the National Academy of Sciences of the United States of America 277 9501169
2016 CREBBP Inactivation Promotes the Development of HDAC3-Dependent Lymphomas. Cancer discovery 215 27733359
2013 Deacetylase-independent function of HDAC3 in transcription and metabolism requires nuclear receptor corepressor. Molecular cell 202 24268577
2006 HDAC3 is crucial in shear- and VEGF-induced stem cell differentiation toward endothelial cells. The Journal of cell biology 195 16982804
2020 Microbiota-derived metabolite promotes HDAC3 activity in the gut. Nature 191 32731255
2024 TRAP1 drives smooth muscle cell senescence and promotes atherosclerosis via HDAC3-primed histone H4 lysine 12 lactylation. European heart journal 136 39088352
2020 Selective Inhibition of HDAC3 Targets Synthetic Vulnerabilities and Activates Immune Surveillance in Lymphoma. Cancer discovery 129 31915197
2020 Dichotomous engagement of HDAC3 activity governs inflammatory responses. Nature 119 32760002
2019 Loss of HDAC3 results in nonreceptive endometrium and female infertility. Science translational medicine 119 30626716
2011 HDAC3 and the molecular brake pad hypothesis. Neurobiology of learning and memory 102 21521655
2008 HDAC3 overexpression and colon cancer cell proliferation and differentiation. Molecular carcinogenesis 98 17849419
2023 HDAC3 deficiency protects against acute lung injury by maintaining epithelial barrier integrity through preserving mitochondrial quality control. Redox biology 96 37244125
2022 HOXB13 suppresses de novo lipogenesis through HDAC3-mediated epigenetic reprogramming in prostate cancer. Nature genetics 87 35468964
2015 Insulin and mTOR Pathway Regulate HDAC3-Mediated Deacetylation and Activation of PGK1. PLoS biology 84 26356530
2019 LncRNA TUG1 mediates ischemic myocardial injury by targeting miR-132-3p/HDAC3 axis. American journal of physiology. Heart and circulatory physiology 79 31858814
2023 HDAC3 aberration-incurred GPX4 suppression drives renal ferroptosis and AKI-CKD progression. Redox biology 77 37890360
2023 TGF-β1/SMAD3 Regulates Programmed Cell Death 5 That Suppresses Cardiac Fibrosis Post-Myocardial Infarction by Inhibiting HDAC3. Circulation research 72 37345556
2019 HDAC3 Deficiency Promotes Liver Cancer through a Defect in H3K9ac/H3K9me3 Transition. Cancer research 71 31097476
2017 HDAC3 regulates DNMT1 expression in multiple myeloma: therapeutic implications. Leukemia 69 28490812
2017 HDAC1 and HDAC3 underlie dynamic H3K9 acetylation during embryonic neurogenesis and in schizophrenia-like animals. Journal of cellular physiology 67 28300292
2015 Hdac3 Deficiency Increases Marrow Adiposity and Induces Lipid Storage and Glucocorticoid Metabolism in Osteochondroprogenitor Cells. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 64 26211746
2018 The HDAC3-SMARCA4-miR-27a axis promotes expression of the PAX3:FOXO1 fusion oncogene in rhabdomyosarcoma. Science signaling 61 30459282
2021 NADPH levels affect cellular epigenetic state by inhibiting HDAC3-Ncor complex. Nature metabolism 59 33462516
2023 HDAC3 Inhibition Promotes Antitumor Immunity by Enhancing CXCL10-Mediated Chemotaxis and Recruiting of Immune Cells. Cancer immunology research 56 36898011
2020 HDAC3 Mediates the Inflammatory Response and LPS Tolerance in Human Monocytes and Macrophages. Frontiers in immunology 56 33123128
2023 The role of HDAC3 and its inhibitors in regulation of oxidative stress and chronic diseases. Cell death discovery 53 37072432
2019 HDAC3 modulates cancer immunity via increasing PD-L1 expression in pancreatic cancer. Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] 50 30670333
2015 Programmed cell death 5 mediates HDAC3 decay to promote genotoxic stress response. Nature communications 47 26077467
2021 HDAC3 inhibitor suppresses endothelial-to-mesenchymal transition via modulating inflammatory response in atherosclerosis. Biochemical pharmacology 45 34339713
2024 Arresting the bad seed: HDAC3 regulates proliferation of different microglia after ischemic stroke. Science advances 44 38446877
2023 Intestinal epithelial HDAC3 and MHC class II coordinate microbiota-specific immunity. The Journal of clinical investigation 43 36602872
2023 Hepatic HDAC3 Regulates Systemic Iron Homeostasis and Ferroptosis via the Hippo Signaling Pathway. Research (Washington, D.C.) 43 38034086
2019 Hdac3, Setdb1, and Kap1 mark H3K9me3/H3K14ac bivalent regions in young and aged liver. Aging cell 43 31858687
2025 A Feedback Loop Driven by H4K12 Lactylation and HDAC3 in Macrophages Regulates Lactate-Induced Collagen Synthesis in Fibroblasts Via the TGF-β Signaling. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 42 39945346
2021 HDAC3 controls male fertility through enzyme-independent transcriptional regulation at the meiotic exit of spermatogenesis. Nucleic acids research 42 33939832
2017 Hdac3 regulates lymphovenous and lymphatic valve formation. The Journal of clinical investigation 42 29035278
2014 PINK1 positively regulates HDAC3 to suppress dopaminergic neuronal cell death. Human molecular genetics 42 25305081
2021 KDELR2 promotes breast cancer proliferation via HDAC3-mediated cell cycle progression. Cancer communications (London, England) 41 34146461
2020 HDAC3 functions as a positive regulator in Notch signal transduction. Nucleic acids research 40 32107550
2019 The HDAC3 enzymatic activity regulates skeletal muscle fuel metabolism. Journal of molecular cell biology 40 30428023
2019 PP4-dependent HDAC3 dephosphorylation discriminates between axonal regeneration and regenerative failure. The EMBO journal 40 31268609
2016 miR-1236 regulates hypoxia-induced epithelial-mesenchymal transition and cell migration/invasion through repressing SENP1 and HDAC3. Cancer letters 39 27177472
2016 HDAC3 mediates smoking-induced pancreatic cancer. Oncotarget 37 26745602
2011 Circadian epigenomic remodeling and hepatic lipogenesis: lessons from HDAC3. Cold Spring Harbor symposia on quantitative biology 37 21900149
2004 Expression and functional characterization of recombinant human HDAC1 and HDAC3. Life sciences 37 15043985
2023 HDAC3 and HDAC8 PROTAC dual degrader reveals roles of histone acetylation in gene regulation. Cell chemical biology 36 37572669
2023 Targeting HDAC3 to overcome the resistance to ATRA or arsenic in acute promyelocytic leukemia through ubiquitination and degradation of PML-RARα. Cell death and differentiation 34 36894687
2018 Lentivirus-Mediated HDAC3 Inhibition Attenuates Oxidative Stress in APPswe/PS1dE9 Mice. Journal of Alzheimer's disease : JAD 34 29376873
2018 Deregulated expression of HDAC3 in colorectal cancer and its clinical significance. Advances in clinical and experimental medicine : official organ Wroclaw Medical University 33 29558042
2022 Epicardial HDAC3 Promotes Myocardial Growth Through a Novel MicroRNA Pathway. Circulation research 32 35722872
2022 Targeting mTORC2/HDAC3 Inhibits Stemness of Liver Cancer Cells Against Glutamine Starvation. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 31 35187863
2020 HDAC3 deteriorates colorectal cancer progression via microRNA-296-3p/TGIF1/TGFβ axis. Journal of experimental & clinical cancer research : CR 30 33203425
2019 HDAC3 Regulates Gingival Fibroblast Inflammatory Responses in Periodontitis. Journal of dental research 29 31693860
2024 The role of HDAC3 in inflammation: mechanisms and therapeutic implications. Frontiers in immunology 27 39050859
2023 Pharmacological blockade of HDAC3 accelerates diabetic wound healing by regulating macrophage activation. Life sciences 27 36931496
2021 HDAC3 Activity within the Nucleus Accumbens Regulates Cocaine-Induced Plasticity and Behavior in a Cell-Type-Specific Manner. The Journal of neuroscience : the official journal of the Society for Neuroscience 27 33602824
2009 The D(3) dopamine receptor inhibits dopamine release in PC-12/hD3 cells by autoreceptor signaling via PP-2B, CK1, and Cdk-5. Journal of neurochemistry 27 19522735
2023 HDAC3 promotes macrophage pyroptosis via regulating histone deacetylation in acute lung injury. iScience 26 37404376
2023 Insights into the function of HDAC3 and NCoR1/NCoR2 co-repressor complex in metabolic diseases. Frontiers in molecular biosciences 25 37674539
2019 EGFR-c-Src-Mediated HDAC3 Phosphorylation Exacerbates Invasion of Breast Cancer Cells. Cells 25 31430896
2024 Kaempferol alleviates myocardial ischemia injury by reducing oxidative stress via the HDAC3-mediated Nrf2 signaling pathway. Journal of advanced research 24 39505146
2023 The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury. Cell death & disease 24 37735154
2022 HDAC3 promotes pulmonary fibrosis by activating NOTCH1 and STAT1 signaling and up-regulating inflammasome components AIM2 and ASC. Cytokine 24 35306425
2021 Histone deacetylase 3 (HDAC3) as an important epigenetic regulator of kidney diseases. Journal of molecular medicine (Berlin, Germany) 24 34698870
2023 Sodium Butyrate Ameliorates Atopic Dermatitis-Induced Inflammation by Inhibiting HDAC3-Mediated STAT1 and NF-κB Pathway. Inflammation 23 38159175
2020 The multifunctional protein PACS-1 is required for HDAC2- and HDAC3-dependent chromatin maturation and genomic stability. Oncogene 23 31988453
2024 Pterostilbene improves neurological dysfunction and neuroinflammation after ischaemic stroke via HDAC3/Nrf1-mediated microglial activation. Cellular & molecular biology letters 22 39198723
2021 The crosstalk of HDAC3, microRNA-18a and ADRB3 in the progression of heart failure. Cell & bioscience 22 33549119
2018 Role of HDAC3-miRNA-CAGE Network in Anti-Cancer Drug-Resistance. International journal of molecular sciences 22 30583572
2007 Benzene's metabolites alter c-MYB activity via reactive oxygen species in HD3 cells. Toxicology and applied pharmacology 22 17614109
2025 Inflammation-driven NF-κB signaling represses ferroportin transcription in macrophages via HDAC1 and HDAC3. Blood 21 39656097
2018 HDAC3-Selective Inhibition Activates Brown and Beige Fat Through PRDM16. Endocrinology 21 29757434
2020 DBC1, p300, HDAC3, and Siah1 coordinately regulate ELL stability and function for expression of its target genes. Proceedings of the National Academy of Sciences of the United States of America 20 32152128
2020 Dynamic Expression of HDAC3 in db/db Mouse RGCs and Its Relationship with Apoptosis and Autophagy. Journal of diabetes research 20 32190700
2020 HDAC3 deacetylates the DNA mismatch repair factor MutSβ to stimulate triplet repeat expansions. Proceedings of the National Academy of Sciences of the United States of America 20 32900932
2022 c-Myc Targets HDAC3 to Suppress NKG2DL Expression and Innate Immune Response in N-Type SCLC through Histone Deacetylation. Cancers 19 35158730
2022 HDAC3 of dorsal hippocampus induces postoperative cognitive dysfunction in aged mice. Behavioural brain research 18 35810999
2019 Coordinated expression of p300 and HDAC3 upregulates histone acetylation during dentinogenesis. Journal of cellular biochemistry 18 31692090
2018 PIWIL2 suppresses Siah2-mediated degradation of HDAC3 and facilitates CK2α-mediated HDAC3 phosphorylation. Cell death & disease 18 29555935
2023 The lysine methyltransferase SMYD2 facilitates neointimal hyperplasia by regulating the HDAC3-SRF axis. Acta pharmaceutica Sinica. B 17 38322347
2019 Mdm2 is required for HDAC3 monoubiquitination and stability. Biochemical and biophysical research communications 17 31358320
2019 The Bdnf and Npas4 genes are targets of HDAC3-mediated transcriptional repression. BMC neuroscience 17 31883511
2018 Clinicopathological features and prediction values of HDAC1, HDAC2, HDAC3, and HDAC11 in classical Hodgkin lymphoma. Anti-cancer drugs 17 29481474
1993 Expression and loss of the transferrin receptor in growing and differentiating HD3 cells. Journal of cellular physiology 17 8482727
2024 Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury. Journal of neuroinflammation 16 38997746
2022 FOXA1 can be modulated by HDAC3 in the progression of epithelial ovarian carcinoma. Journal of translational medicine 16 34991620
2022 Inhibition of HDAC3 and ATXN3 by miR-25 prevents neuronal loss and ameliorates neurological recovery in cerebral stroke experimental rats. Journal of physiology and biochemistry 16 35025075
2022 Depleted HDAC3 attenuates hyperuricemia-induced renal interstitial fibrosis via miR-19b-3p/SF3B3 axis. Cell cycle (Georgetown, Tex.) 16 35025700
2020 Aberrant HDAC3 expression correlates with brain metastasis in breast cancer patients. Thoracic cancer 16 32686908
2020 Hdac3 regulates bone modeling by suppressing osteoclast responsiveness to RANKL. The Journal of biological chemistry 15 33454009
2022 Inhibition of HDAC3 protects against kidney cold storage/transplantation injury and allograft dysfunction. Clinical science (London, England : 1979) 14 34918039
2019 HDAC3 positively regulates HE4 expression to promote ovarian carcinoma progression. Archives of biochemistry and biophysics 14 31302139
2018 Tyrosine phosphorylation of HDAC3 by Src kinase mediates proliferation of HER2-positive breast cancer cells. Journal of cellular physiology 14 30317579
2004 The effects of benzene and the metabolites phenol and catechol on c-Myb and Pim-1 signaling in HD3 cells. Toxicology and applied pharmacology 14 15541759
2023 Circular RNA ACACA negatively regulated p53-modulated mevalonate pathway to promote colorectal tumorigenesis via regulating miR-193a/b-3p/HDAC3 axis. Molecular carcinogenesis 13 36920044
2024 HDAC3 genetic and pharmacologic inhibition radiosensitizes fusion positive rhabdomyosarcoma by promoting DNA double-strand breaks. Cell death discovery 12 39107280
2023 Novel mechanism for zinc inducing hepatic lipolysis via the HDAC3-mediated deacetylation of β-catenin at lysine 311. The Journal of nutritional biochemistry 12 37591442
2020 Targeting HDAC3 in the DBA/2J spontaneous mouse model of glaucoma. Experimental eye research 12 32971093

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