Affinage

HDAC5

Histone deacetylase 5 · UniProt Q9UQL6

Length
1122 aa
Mass
122.0 kDa
Annotated
2026-06-10
100 papers in source corpus 49 papers cited in narrative 49 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

HDAC5 is a signal-responsive class IIa histone deacetylase that functions principally as a transcriptional co-repressor, binding MEF2 family transcription factors through its N-terminal non-deacetylase domain to inhibit their activity in a deacetylase-independent manner (PMID:10748098). This MEF2 axis governs diverse differentiation and stress programs: HDAC5 represses the PGC-1α promoter to control cardiac mitochondrial biogenesis (PMID:12578979), suppresses a distal SOST enhancer in osteocytes to regulate bone mass (PMID:25271055), and mediates PTHrP repression of chondrocyte hypertrophy (PMID:30843886). The gene-regulatory output of HDAC5 is set by phosphorylation-dependent nucleocytoplasmic shuttling: multiple kinases—CaMK (PMID:12641737, PMID:20042720), PKD (PMID:19124542), SIK1 (PMID:18946175), PKCα/PKCμ (PMID:21642422, PMID:24209626), and FAK (at Tyr642) (PMID:32612176)—phosphorylate Ser259/Ser498 to drive cytoplasmic export and MEF2 de-repression, while B55α/PP2A-mediated dephosphorylation promotes nuclear retention (PMID:28343149). Beyond MEF2, HDAC5 acts as a co-repressor or scaffold for numerous partners including GATA1 (PMID:14668799), YY1 (PMID:18632988), p53 (PMID:24120667), PPARα (PMID:29229738), and RB (PMID:33419772). In the cytoplasm HDAC5 functions as an injury-regulated tubulin deacetylase, acting through filamin A to drive growth cone dynamics and peripheral axon regeneration (PMID:22692128, PMID:26157139). HDAC5 additionally deacetylates non-histone substrates including p53 at K120 (PMID:24120667), Hsp70 to stabilize HIF-1α (PMID:26061431), NF-κB p65 at K310 (PMID:35265200), GATA1 (PMID:36102738), and STAT6 (PMID:40250791), placing it at the intersection of calcium signaling, energy sensing, mechanotransduction, and epigenetic control of metabolism, differentiation, and stress responses.

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2000 High

    Established the founding mechanism of HDAC5 as a MEF2 co-repressor and showed, unexpectedly, that repression does not require the catalytic deacetylase domain.

    Evidence Reciprocal Co-IP, domain mapping, and reporter assays defining the HDAC5–MEF2A interaction

    PMID:10748098

    Open questions at the time
    • Mechanism of deacetylase-independent repression not resolved
    • Did not address how the interaction is regulated by signaling
  2. 2003 High

    Connected HDAC5 to a physiological output by showing it represses the MEF2/PGC-1α axis controlling cardiac mitochondrial biogenesis, and that signal-resistant HDAC5 produces a defined in vivo phenotype.

    Evidence Transgenic mouse expressing phosphorylation-defective HDAC5 plus PGC-1α promoter analysis

    PMID:12578979

    Open questions at the time
    • Did not identify the kinase(s) normally relieving repression
    • Restricted to cardiac tissue
  3. 2003 High

    Demonstrated that signaling (calcium/CaMK) physically relocates HDAC5 between nucleus and cytoplasm, establishing the shuttling paradigm that governs its co-repressor function.

    Evidence Live imaging of GFP-HDAC5 in neurons with calcium channel and CaMK pharmacology; Co-IP/co-localization with GATA1 in erythroleukemia cells

    PMID:12641737 PMID:14668799

    Open questions at the time
    • Exact phospho-acceptor residues not yet mapped in these studies
    • GATA1 work was correlative for differentiation
  4. 2005 Medium

    Showed that HDAC5 co-repressor activity is gated by direct protein binding as well as phosphorylation, expanding the regulatory repertoire to G protein and additional transcription factor inputs.

    Evidence Y2H, Co-IP, and MEF2C reporter assays for Gβγ binding; Co-IP and kinase/phosphatase manipulation for YY1, GEF, and AhRR/ANKRA2 partnerships

    PMID:16221676 PMID:16822951 PMID:17949687 PMID:18216015 PMID:18632988

    Open questions at the time
    • Several partner interactions rest on single-lab Co-IP
    • Relative physiological weighting of these partners unclear
  5. 2009 High

    Mapped the regulated phospho-acceptor sites (Ser259/Ser498) and tied diverse upstream signals—shear stress, adrenergic, salt-inducible kinase—to HDAC5 export and target gene activation.

    Evidence Phospho-site mutant (S259A/S498A) analysis with functional readouts in endothelial cells, muscle fibers, and myoblasts; SIK1/GIT1 kinase pathway dissection

    PMID:18292392 PMID:18946175 PMID:19124542 PMID:20042720

    Open questions at the time
    • Combinatorial logic among kinases not fully resolved
    • Site-specific phosphatase activity not yet defined here
  6. 2012 High

    Revealed cytoplasmic catalytic functions of HDAC5 distinct from transcriptional repression, including injury-induced tubulin deacetylation driving axon regeneration and a role in heterochromatin replication.

    Evidence In vitro and in vivo nerve injury models with PKC inhibition and acetylated-tubulin readout; RNAi with replication fork and DNA damage assays

    PMID:22301920 PMID:22648949 PMID:22692128

    Open questions at the time
    • Why peripheral but not central neurons activate the pathway not mechanistically resolved at this stage
    • Heterochromatin role lacks direct substrate identification
  7. 2013 High

    Established HDAC5 as a non-histone substrate deacetylase and scaffold, deacetylating p53 at K120 to gate apoptosis and bridging HDAC1/Sin3a co-repressors to cardiac transcription factors.

    Evidence Co-IP, ChIP, acetylation assays, and in vivo knockdown for p53; HDAC5 KO mice with ChIP/Co-IP for Nkx2.5/YY1 scaffolding and alternative splicing

    PMID:23424201 PMID:24120667 PMID:24209626 PMID:26704971

    Open questions at the time
    • Substrate specificity determinants for K120 deacetylation not defined
    • Scaffold versus catalytic contributions not cleanly separated
  8. 2015 High

    Defined HDAC5 as a node coupling energy/mechanical signaling to epigenetic and non-histone outputs, including Hsp70 deacetylation stabilizing HIF-1α and filamin A-dependent tubulin deacetylation.

    Evidence AMPK manipulation with Hsp70 deacetylation and HIF-1α fractionation; ChIP at the SOST enhancer with KO mice; filamin A Co-IP and axon regeneration assays

    PMID:24732133 PMID:25271055 PMID:26061431 PMID:26157139

    Open questions at the time
    • Compensation by PKD when AMPK is lost complicates pathway assignment
    • Direct structural basis of substrate engagement unknown
  9. 2017 High

    Identified the phosphatase arm of the shuttling switch (B55α/PP2A) and extended the regulatory output to liver fatty acid oxidation via PPARα and to behavioral/addiction circuits via Npas4.

    Evidence Co-IP and B55α knockdown defining the dephosphorylation step; PPARα Co-IP with phospho-mutant mice; ChIP at Npas4 enhancer with conditional KO and behavior

    PMID:26647181 PMID:28343149 PMID:28957664 PMID:29229738

    Open questions at the time
    • Tissue-specific selection of phosphatase versus kinase inputs incompletely mapped
    • How nuclear HDAC5 distinguishes activating versus repressive partners unclear
  10. 2019 High

    Added a tyrosine-phosphorylation arm (FAK at Tyr642) controlling localization in mechanically loaded osteocytes and resolved redundancy with HDAC4 across cardiac, skeletal, and developmental contexts.

    Evidence Phospho-Tyr immunoblotting, Tyr642 mutagenesis, and FAK inhibition in vitro and in vivo; HDAC4/HDAC5 single and double KO models

    PMID:30843886 PMID:30910408 PMID:31696766 PMID:32485181 PMID:32612176

    Open questions at the time
    • Crosstalk between Ser and Tyr phosphorylation not integrated
    • Degree of HDAC4/HDAC5 functional overlap is context-dependent and not generalized
  11. 2022 High

    Cemented HDAC5 as a cancer-relevant deacetylase acting on RB, NF-κB p65, GATA1, and STAT6 to drive proliferation, immune evasion, metabolic rewiring, and therapy resistance.

    Evidence Motif mutagenesis and H3K27ac ChIP for RB; deacetylation assays and in vivo models for p65-K310, GATA1, and SOX9; SIK1/14-3-3/TRIM28 stabilization with STAT6 deacetylation

    PMID:27212032 PMID:30151243 PMID:31690832 PMID:33377659 PMID:33419772 PMID:35265200 PMID:35396379 PMID:36102738 PMID:40250791

    Open questions at the time
    • Which substrates dominate in a given tumor context unresolved
    • Catalytic versus scaffolding contributions to oncogenic output not always separated

Open questions

Synthesis pass · forward-looking unresolved questions
  • How HDAC5 selects among its many partners and substrates within a single cell, and the structural basis for its deacetylase-independent repression, remain unresolved.
  • No structural model for partner/substrate discrimination
  • Integration of Ser259/Ser498 versus Tyr642 phosphorylation codes not defined
  • Catalytic versus scaffolding roles not cleanly partitioned across contexts

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 6 GO:0060090 molecular adaptor activity 2 GO:0140098 catalytic activity, acting on RNA 2
Localization
GO:0005634 nucleus 6 GO:0005829 cytosol 5 GO:0000228 nuclear chromosome 1
Pathway
R-HSA-162582 Signal Transduction 5 R-HSA-74160 Gene expression (Transcription) 5 R-HSA-1430728 Metabolism 4 R-HSA-1643685 Disease 4 R-HSA-4839726 Chromatin organization 4
Partners
FLNAGATA1MEF2AMEF2CP53PPARARB1YY1
Complex memberships
AhRR/ANKRA2/HDAC5 co-repressorHDAC4/5-DREAM complexNuRSERY (HDAC5/GATA1/EKLF/pERK)

Evidence

Reading pass · 49 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 HDAC5 physically interacts with MEF2A in vivo and in vitro and strongly inhibits its transcriptional activity. The repression is independent of the HDAC5 deacetylase domain; the N-terminal non-deacetylase domain is sufficient for repression. The MADS box/MEF2-domain region of MEF2A interacts with a limited region in the N-terminal part of HDAC5. Co-immunoprecipitation (in vivo and in vitro), domain mapping, transcriptional reporter assays The Journal of biological chemistry High 10748098
2003 HDAC5 represses PGC-1α transcription through MEF2-binding sites in the PGC-1α promoter. Transgenic expression of a signal-resistant (phosphorylation-defective) HDAC5 in mouse heart causes loss of cardiac mitochondria, down-regulation of mitochondrial enzymes, and down-regulation of PGC-1α, placing HDAC5 as a repressor of the MEF2/PGC-1α axis controlling cardiac mitochondrial biogenesis. Transgenic mouse model (signal-resistant HDAC5), promoter analysis, transcriptional reporter assay Proceedings of the National Academy of Sciences of the United States of America High 12578979
2003 Neuronal activity controls the nucleocytoplasmic distribution of HDAC5 in hippocampal neurons. HDAC5 nuclear export requires stimulation of calcium flux through synaptic NMDA receptors or L-type calcium channels and is sensitive to the CaM kinase inhibitor KN-62, establishing that CaMK signaling drives HDAC5 cytoplasmic translocation in neurons. Live-cell imaging of GFP-tagged HDAC5, pharmacological inhibitors (KN-62), calcium channel blockers Journal of neurochemistry High 12641737
2003 HDAC5 directly associates with GATA-1 and co-localizes with it in the nucleus of murine erythroleukemia (MEL) cells. Co-expression of HDAC5 suppresses GATA-1 transcriptional activity. During HMBA-induced erythroid differentiation a portion of HDAC5 relocates to the cytoplasm, correlated with de-repression of GATA-1. Co-immunoprecipitation, co-localization by immunofluorescence, transcriptional reporter assay, subcellular fractionation Oncogene Medium 14668799
2005 Gβγ subunit of heterotrimeric G proteins directly binds HDAC5 through its C-terminal domain. This interaction occurs in a signal-dependent manner, can be blocked by Gαo overexpression and reversed by α2A-adrenergic receptor activation. Formation of the Gβ1γ2–HDAC5 complex inhibits HDAC5-mediated transcriptional co-repression of MEF2C, indicating that G protein signaling directly controls HDAC5 co-repressor function. Yeast two-hybrid screen, co-immunoprecipitation in mammalian cells, MEF2C transcriptional reporter assay, Gβγ scavenger overexpression The Journal of biological chemistry Medium 16221676
2006 HDAC5 localization in H9C2 cells is controlled by CaMKIV and/or PKD (which maintain cytoplasmic HDAC5 in undifferentiated cells) and by PP2A phosphatase (which promotes nuclear HDAC5 in differentiated cells). In differentiated cells, nuclear HDAC5 interacts with YY1 transcription factor and is required for YY1 repressor function. GFP-fusion live imaging, co-immunoprecipitation, dominant-negative kinase/phosphatase constructs American journal of physiology. Cell physiology Medium 16822951
2007 HDAC5 is recruited as a co-repressor to the CYP1A1 promoter via interaction with AhRR and the adaptor protein ANKRA2 (which bridges HDAC4/5 to AhRR). RNA interference of ANKRA2 or AhRR reduces this repression, establishing an AhRR/ANKRA2/HDAC5 co-repressor axis. Yeast two-hybrid, RNAi knockdown, chromatin immunoprecipitation, transcriptional reporter assay Biochemical and biophysical research communications Medium 17949687
2008 SIK1 (salt-inducible kinase 1) phosphorylates HDAC5 causing its nuclear export and activation of MEF2C in AICAR-treated C2C12 myoblasts. GSK-3β contributes to sustained SIK1 activity, and this pathway drives PGC-1α expression in a HDAC5/MEF2C-dependent manner. In vitro kinase assay, GFP-HDAC5 nuclear export imaging, dominant-negative constructs, pharmacological inhibitors Endocrine journal Medium 18946175
2008 YY1 transcription factor interacts with HDAC5 via the HDAC5 phosphorylation domain and prevents HDAC5 nuclear export in response to hypertrophic stimuli in cardiac myocytes. The interaction is required for YY1 to function as a transcription repressor; YY1 overexpression reduces HDAC5 phosphorylation in response to hypertrophic stimuli. Co-immunoprecipitation, GFP-HDAC5 localization, siRNA knockdown, dominant-negative and deletion constructs, luciferase reporter assays Molecular biology of the cell Medium 18632988
2008 GIT1 scaffold protein mediates Ang II-induced phosphorylation of HDAC5 at Ser498 in vascular smooth muscle cells through a Src–PLCγ–CaMKII signaling pathway. Knockdown of GIT1 decreases Ang II-induced HDAC5 phosphorylation and MEF2 transcriptional activity. siRNA knockdown, phospho-specific antibodies, co-immunoprecipitation of GIT1-CaMKII, MEF2 reporter assays Arteriosclerosis, thrombosis, and vascular biology Medium 18292392
2008 HDAC5 interacts with GEF (GLUT4 enhancer factor) in the absence of MEF2 proteins and specifically inhibits GLUT4 promoter activity through this interaction. Co-immunoprecipitation, GLUT4 promoter luciferase reporter assay The Journal of biological chemistry Low 18216015
2009 Fluid shear stress stimulates CaMK-dependent phosphorylation of HDAC5 at Ser259/Ser498 and its nuclear export in endothelial cells, causing dissociation from MEF2 and MEF2-driven expression of KLF2 and eNOS. A phosphorylation-defective HDAC5 mutant (S259A/S498A) blocks these effects and attenuates the anti-inflammatory response. Adenoviral overexpression of HDAC5-S/A mutant, phospho-specific immunoblotting, MEF2 reporter assay, cell adhesion assay Blood High 20042720
2009 Alpha-adrenergic receptor activation by phenylephrine causes PKD-dependent HDAC5 nuclear efflux in slow soleus skeletal muscle fibers. PKD1 redistribution and HDAC5 export are transient (reflecting receptor desensitization), whereas phorbol ester (PMA) causes continuous PKD-dependent export. This HDAC5 export increases histone H3 acetylation and MEF2 reporter activity. Live-cell imaging of HDAC5-GFP and PKD1-mPlum in isolated adult muscle fibers, pharmacological inhibition, histone acetylation immunoblot, MEF2 reporter assay The Journal of physiology Medium 19124542
2011 In vascular smooth muscle cells (VSMCs), CaMKIIδ2 mediates Ca2+-dependent phosphorylation of both HDAC4 and HDAC5 in response to AngII and PDGF. HDAC5 regulation depends on HDAC4: suppression of HDAC4 expression and activity prevents AngII/PDGF-dependent phosphorylation of HDAC5. This regulates MEF2 DNA-binding and target gene expression (Nur77, MCP1). CaMKIIδ2 siRNA/dominant-negative, HDAC4 siRNA, phospho-HDAC immunoblots, MEF2 DNA-binding ELISA, qPCR The Biochemical journal Medium 22360269
2011 Calpain-generated free catalytic domain of PKCα (PKCα-CT) constitutively localizes to nuclei and directly drives nucleocytoplasmic shuttling of HDAC5, inducing MEF2-dependent inflammatory pathway gene expression. This occurs independently of PKD, which is required for receptor-mediated (phorbol ester) HDAC5 export. Confocal imaging of nuclear/cytoplasmic HDAC5, adenoviral PKCα-CT expression, PKD inhibition, gene expression analysis The Journal of biological chemistry Medium 21642422
2012 HDAC5 is associated with actively replicating pericentric heterochromatin during late S phase. RNAi-mediated depletion of HDAC5 disrupts heterochromatin structure, slows replication forks, triggers DNA damage checkpoint activation, and induces autophagy and apoptosis in cancer cells in vitro and in vivo. RNAi knockdown, BrdU incorporation/replication fork assay, immunofluorescence, xenograft tumor assay Cell death and differentiation Medium 22301920
2012 HDAC5 functions as an injury-regulated tubulin deacetylase in peripheral neurons. Axon injury induces calcium influx that activates PKC-mediated HDAC5 activity at the injury site, leading to localized tubulin deacetylation. This is required for growth cone dynamics and axon regeneration in vitro and in vivo; central neurons fail to activate this pathway. In vitro axon regeneration assays, in vivo sciatic nerve injury model, pharmacological PKC inhibition, HDAC5 knockdown/overexpression, acetylated tubulin immunostaining The EMBO journal High 22692128
2012 NOX2-derived reactive oxygen species (ROS) drive HDAC5 nuclear efflux during intense (50 Hz) repetitive stimulation of fast skeletal muscle fibers. This is completely blocked by ROS scavenger NAC and absent in NOX2 knockout fibers, in contrast to HDAC4 efflux which is additionally regulated by CaMK. GFP-HDAC5 live imaging in isolated muscle fibers, NAC scavenger treatment, NOX2 knockout mice, KN-62 CaMK inhibition American journal of physiology. Cell physiology High 22648949
2013 Axon injury in peripheral sensory neurons elicits a back-propagating calcium wave that causes PKCμ-dependent nuclear export of HDAC5, thereby enhancing histone acetylation and activating a pro-regenerative gene-expression program. A nuclear-trapped HDAC5 mutant prevents axon regeneration; enhancing HDAC5 nuclear export promotes regeneration in vitro and in vivo. This pathway fails to activate in central nervous system injury. Calcium imaging, PKCμ inhibition/knockdown, HDAC5 nuclear-trap mutant expression, in vivo sciatic nerve injury regeneration assay, gene expression profiling Cell High 24209626
2013 HDAC5 binds to p53 and abrogates acetylation of p53 at K120. This prevents p53 recruitment to pro-apoptotic gene promoters at early phases of genotoxic stress, promoting arrest/antioxidant gene expression. Upon prolonged stress, HDAC5 undergoes nuclear export, p53 becomes K120-acetylated, and pro-apoptotic genes are selectively transactivated. Co-immunoprecipitation, chromatin immunoprecipitation, acetylation assays, HDAC5 knockdown in mice, gene expression analysis Molecular cell High 24120667
2013 HDAC5 interacts with Tbx3 transcription factor via two critical motifs (585LFSYPYT591 and 604HRH606) and mediates Tbx3-driven repression of E-cadherin and HCC cell migration/metastasis. An HDAC inhibitor blocks Tbx3-mediated E-cadherin downregulation. Glycine scan mutagenesis, deletion assays, co-immunoprecipitation, E-cadherin promoter reporter, in vitro migration assay, in vivo metastasis assay Signal transduction and targeted therapy Medium 30151243
2013 HDAC5 is required for the interaction of HDAC1/2/Sin3a co-repressor complexes with transcription factors Nkx2.5 and YY1 at the Ncx1 and Bnp promoters in heart. HDAC5 knockout prevents pressure overload-induced Ncx1 upregulation and prevents recruitment of HDAC1/Sin3a co-repressor to these promoters, supporting a non-canonical scaffolding role for HDAC5. HDAC5 knockout mouse, pressure overload model, co-immunoprecipitation, chromatin immunoprecipitation Nucleic acids research Medium 26704971
2013 HDAC5-deficient mice have reduced cardiac PTB protein abundance. HDAC inhibition in myocytes reduces cFLIP expression, enabling caspase-dependent PTB cleavage. This pathway controls alternative splicing of tropomyosin-1, tropomyosin-2, and MEF2 in the developing heart. HDAC5 knockout mouse, cFLIP overexpression, caspase inhibition, in vitro caspase cleavage assay, RT-PCR for alternative splicing Journal of cell science Medium 23424201
2014 HDAC5 in erythroid cells forms a novel complex (NuRSERY) with GATA1, EKLF, and pERK, as identified by pull-down experiments. ERK phosphorylation is required for complex formation; inhibition of ERK phosphorylation reduces nuclear content of HDAC5, GATA1, and EKLF by >90%. The complex is erythroid-specific and regulates globin gene expression. Co-immunoprecipitation/pulldown, pharmacological ERK inhibition, class IIa-selective HDAC inhibitor, RT-PCR for globin expression The international journal of biochemistry & cell biology Medium 24594363
2015 HDAC5 negatively regulates sclerostin (SOST) expression in osteocytes by binding and inhibiting MEF2C. ChIP mapping identified MEF2C binding at a distal SOST enhancer 45 kb downstream of the transcription start site. HDAC5 deficiency increases MEF2C chromatin association at this enhancer, increases H3K27ac, and decreases NCoR/HDAC3 co-repressor recruitment. HDAC5 knockout mice show increased SOST mRNA and sclerostin protein, decreased Wnt activity, and reduced bone mass. HDAC5 shRNA/overexpression, HDAC5 knockout mice, chromatin immunoprecipitation (ChIP), MEF2C knockdown rescue experiment Journal of bone and mineral research High 25271055
2015 HDAC5 deacetylates cytosolic Hsp70, which reduces Hsp70 affinity for HIF-1α, thereby decreasing HIF-1α degradation and enabling its nuclear accumulation. AMPK activation promotes cytoplasmic shuttling of HDAC5 which is necessary for this activity under hypoxia or low glucose. HDAC5 knockdown impairs hypoxia-induced HIF-1α accumulation. HDAC5 knockdown/overexpression, Hsp70 co-immunoprecipitation, acetylation assay of Hsp70, AMPK inhibition, HIF-1α nuclear fractionation Cell cycle (Georgetown, Tex.) Medium 26061431
2015 Ketamine rapidly stimulates HDAC5 phosphorylation and nuclear export in rat hippocampal neurons through CaMKII- and PKD-dependent pathways, enhancing MEF2 transcriptional activity. A phosphorylation-defective HDAC5 mutant (S259A/S498A) blocks ketamine-induced MEF2 activation. Hippocampal knockdown of HDAC5 blocks the antidepressant-like effects of ketamine in rats. Phospho-specific immunoblotting, GFP-HDAC5 nuclear export imaging, HDAC5-S/A adenovirus, viral-mediated hippocampal knockdown, behavioral assays Proceedings of the National Academy of Sciences of the United States of America High 26647181
2015 Filamin A interacts with HDAC5 via its C-terminal domain and is required for HDAC5-dependent tubulin deacetylation at the injury site. Filamin A axonal expression increases after nerve injury in a protein synthesis-dependent manner. Disruption of the HDAC5–filamin A interaction prevents injury-induced tubulin deacetylation and reduces axon regeneration. Co-immunoprecipitation, filamin A knockdown, axon regeneration assay, acetylated tubulin immunostaining The Journal of biological chemistry Medium 26157139
2015 AMPK loss in muscle does not affect HDAC5 phosphorylation during exercise; instead, compensatory PKD activation (32.6% increase) maintains HDAC5 phosphorylation. When HDAC5 phosphorylation is blocked in the context of active PKD, alternative post-transcriptional reduction of HDAC5 mRNA and protein occurs, activating a subset of metabolic genes. AMPK knockout mouse, exercise protocol, PKD activity assay, C2C12 cell overexpression, metabolic gene expression analysis FASEB journal Medium 24732133
2016 HDAC5 physically interacts with LSD1 through its domain containing nuclear localization sequence and phosphorylation sites. HDAC5 stabilizes LSD1 protein and promotes USP28 (a deubiquitinase of LSD1) protein stability, decreasing LSD1 ubiquitination/degradation. Loss of HDAC5 diminishes LSD1 demethylase activity and reduces H3K4me1/me2 nuclear levels. Co-immunoprecipitation, HDAC5 deletion mutants, in vitro acetylation assays, siRNA knockdown, LSD1 ubiquitination assay Oncogene Medium 27212032
2017 Dephosphorylated, nuclear HDAC5 in the nucleus accumbens associates with an activity-sensitive enhancer of the Npas4 gene and negatively regulates NPAS4 expression. HDAC5 nuclear activity reduces cocaine reward-context associations; conditional Npas4 deletion in NAc reduces cocaine CPP and delayed drug-reinforced learning. Chromatin immunoprecipitation, conditional Npas4 knockout, viral-mediated HDAC5 overexpression, cocaine self-administration and CPP behavioral paradigms Neuron High 28957664
2017 Fasting glucagon promotes dephosphorylation and nuclear translocation of HDAC5 in liver. Nuclear HDAC5 interacts with PPARα and promotes PPARα transcriptional activity and fatty acid oxidation gene expression. ER stress activates CaMKII-mediated phosphorylation of HDAC5, causing its cytoplasmic retention and impairing fatty acid oxidation. A phosphorylation-deficient HDAC5 mutant (2SA) protects against hepatic steatosis in HFD-fed mice. HDAC5 co-immunoprecipitation with PPARα, liver-specific HDAC5 overexpression/knockdown, phospho-deficient HDAC5 2SA mutant mouse, HFD model, gene expression analysis Journal of lipid research High 29229738
2017 β-Adrenergic stimulation induces HDAC5 nuclear accumulation in cardiomyocytes via a β1-AR/PKA-dependent mechanism. This requires B55α-PP2A-mediated dephosphorylation of Ser259/Ser498 (not Ser279). Co-immunoprecipitation revealed a specific HDAC5–B55α interaction that increases >3-fold with isoproterenol. B55α knockdown attenuates isoproterenol-induced HDAC5 dephosphorylation. 3D confocal microscopy, site-directed mutagenesis (Ser259/279/498), pharmacological PKA/PP2A inhibitors, Co-IP, B55α siRNA knockdown Journal of the American Heart Association High 28343149
2018 CD13 interacts with HDAC5 via co-immunoprecipitation to promote HDAC5 protein stability. Stabilized HDAC5 then deacetylates LSD1, promoting LSD1 stability, which decreases NF-κB p65 methylation and increases p65 stability, activating NF-κB signaling. Co-immunoprecipitation, LC-MS/MS proteomic analysis, LSD1 deacetylation assay, p65 methylation assay Clinical and translational medicine Medium 33377659
2018 HDAC5 interacts with GCM1 transcription factor in placental cells, facilitating GCM1 deacetylation and suppression of its transcriptional activity and syncytin-1 expression/cell fusion. Epac1/Rap1/CaMKI signaling phosphorylates HDAC5 at Ser259/Ser498, causing its nuclear export and de-repression of GCM1 activity. Co-immunoprecipitation, immunofluorescence co-localization, phospho-specific antibodies, RNA interference, cell fusion assay, constitutively active Epac1/CaMKI constructs Molecular human reproduction Medium 23867755
2018 KSHV viral IRF3 (vIRF3) physically interacts with HDAC5 (identified by mass spectrometry) and blocks phosphorylation-dependent cytoplasmic translocation of HDAC5 in lymphatic endothelial cells (LECs), altering global gene expression specifically in LECs (not BECs) and inducing hypersprouting/lymphangiogenesis. Co-immunoprecipitation, mass spectrometry, immunofluorescence, ΔvIRF3 KSHV mutant infection, gene expression analysis mBio Medium 29339432
2018 HDAC5 deacetylates SOX9, which is required for SOX9 nuclear translocation in tamoxifen-resistant breast cancer cells. HDAC5 physically interacts with SOX9 as shown by co-immunoprecipitation. C-MYC transcriptionally promotes HDAC5 expression in resistant cells. Co-immunoprecipitation, acetylation immunoprecipitation, subcellular fractionation, qRT-PCR, siRNA knockdown British journal of cancer Medium 31690832
2019 HDAC4 and HDAC5 form a complex with DREAM transcription factor that is recruited to the ncx3 promoter, causing histone deacetylation and NCX3 gene silencing after stroke. DREAM knockdown prevents HDAC4/5 recruitment to the ncx3 promoter. Pharmacological class IIa HDAC inhibition (MC1568) increases NCX3 expression and reduces neuronal stroke damage. Co-immunoprecipitation, chromatin immunoprecipitation, siRNA knockdown, in vitro OGD model, in vivo tMCAO rat model, class IIa HDAC inhibitor Journal of cerebral blood flow and metabolism Medium 31696766
2019 PTHrP inhibits chondrocyte hypertrophy partly through HDAC5. In mice, HDAC5 KO in addition to HDAC4 KO is required to fully block PTHrP action on chondrocyte differentiation at birth. PTHrP reduces HDAC4 phosphorylation at 14-3-3-binding sites and promotes nuclear translocation of HDAC4/5, which then repress MEF2 activity and Runx2 mRNA expression needed for hypertrophy. Multiple mouse genetic knockout models (Hdac4-KO, Hdac5-KO, double-KO), PTHrP-KO epistasis, phospho-immunoblotting, immunofluorescence JCI insight High 30843886
2019 FAK directly phosphorylates HDAC5 at tyrosine 642, a post-translational modification that controls HDAC5 subcellular localization in osteocytes. Fluid flow shear stress triggers FAK dephosphorylation, driving class IIa HDAC (HDAC4/5) nuclear translocation, which is required for loading-induced SOST suppression and bone formation. Phospho-tyrosine immunoblotting, FAK catalytic inhibitor (in vitro and in vivo), site-directed mutagenesis of Tyr642, Ocy454 cell line FFSS model, mouse loading model Nature communications High 32612176
2019 HDAC5 promotes optic nerve regeneration in RGCs when in its cytoplasmic form. An HDAC5 mutant with Ser259/488 replaced by Ala (predominantly cytoplasmic) stimulates RGC survival and optic nerve regeneration in vivo by activating the mTOR pathway, an effect not seen with wild-type HDAC5. AAV-mediated in vivo HDAC5 and HDAC5AA expression in RGCs, optic nerve crush model, mTOR pathway immunoblotting, immunofluorescence of pS6/RGC markers Experimental neurology Medium 30910408
2019 HDAC5 regulates SOX10 expression by directly binding to the promoter region of the Sox10 gene (as shown by ChIP), thereby upregulating SOX10 and promoting spinal neuronal sensitization in neuropathic pain models. Chromatin immunoprecipitation (ChIP), lentiviral HDAC5 overexpression/knockdown, mechanical allodynia/thermal hyperalgesia behavioral testing, immunoblotting Pain Medium 29447134
2020 HDAC5 regulates PD-L1 expression by directly interacting with NF-κB p65 and deacetylating p65 at lysine-310, which reduces p65 transcriptional activity. This interaction is suppressed by p65 phosphorylation at serine-311. HDAC5 silencing/inhibition sensitizes pancreatic cancer to immune checkpoint blockade in syngeneic and KPC mouse models. Co-immunoprecipitation, p65 deacetylation assay, phospho-mutant p65, syngeneic/KPC allograft tumor models, immune checkpoint blockade combination treatment Theranostics High 35265200
2020 Cyclic AMP (cAMP)/PKA signaling causes nuclear retention and hypo-phosphorylation of HDAC5 (at Ser259/498) and HDAC9 in cardiomyocytes but not non-myocytes, via PKA-dependent inhibition of PKD. Endogenous HDAC5 (but not HDAC9) specifically contributes to repression of endogenous MEF2 activity; cardiomyocytes deficient in both HDAC5 and HDAC4 show blunted cAMP-induced repression of cellular hypertrophy. HDAC5/HDAC9/HDAC4 knockout neonatal cardiomyocytes, 3D confocal localization imaging, PKD inhibition, MEF2 reporter assay, cell size measurement Journal of molecular and cellular cardiology High 32485181
2021 HDAC5 interacts with RB tumor suppressor through an FXXXV motif (with RB-N) and also with RB-C; these interactions are diminished by RB phosphorylation at Ser249/Thr252 and Thr821. HDAC5 loss increases H3K27 acetylation and circumvents RB-mediated repression of cell-cycle-related pro-oncogenic genes, conferring CDK4/6 inhibitor resistance. Co-immunoprecipitation, HDAC5 LXCXE/FXXXV motif mutagenesis, H3K27ac ChIP, HDAC5 KO in prostate/breast cancer cells and in vivo xenograft models Cancer research High 33419772
2022 HDAC5 deacetylates GATA1, which represses cPLA2 expression. HDAC5 knockdown results in hyperacetylation of GATA1, enabling upregulation of cPLA2 and overproduction of arachidonic acid (AA) in pancreatic cancer. This renders HDAC5-deficient tumors sensitive to cPLA2 inhibition. GATA1 acetylation assay by Co-IP/immunoblot, ChIP, cPLA2 promoter analysis, nontargeted metabolomics, cPLA2 genetic/pharmacologic inhibition, in vivo xenograft/dietary manipulation Cancer research High 36102738
2022 HDAC5 interacts with MEF2A and suppresses MEF2A binding to the Smad7 promoter, resulting in Smad7 repression, sustained Smad2/3 phosphorylation, and fibroblast activation in hypertrophic scar. LMK235 (HDAC4/5 inhibitor) alleviates scar formation. Smad7 knockdown rescues the phenotype of HDAC5 deficiency. Co-immunoprecipitation, chromatin immunoprecipitation (ChIP-qPCR), luciferase reporter assay, Smad7 rescue knockdown, in vivo hypertrophic scar model International journal of biological sciences Medium 36263180
2022 HDAC5 reduces the enrichment of H3K9/K14ac on the miR-142 promoter, suppressing miR-142-5p expression and upregulating ARMC8 in osteosarcoma. METTL3 increases m6A on HDAC5 mRNA, stabilizing it and promoting HDAC5-mediated miR-142 repression and OS cell proliferation. m6A-methylation assay, HDAC5 knockdown/overexpression, H3K9/K14ac ChIP, miR-142-5p expression analysis, xenograft tumor model Cell death discovery Medium 35396379
2025 SIK1 phosphorylates HDAC5 at Ser498, promoting its interaction with 14-3-3 protein and protecting it from TRIM28-mediated ubiquitylation/degradation. SIK1-stabilized HDAC5 deacetylates STAT6, enhancing STAT6 transcriptional activity and upregulating SLC7A11, conferring ferroptosis resistance in pancreatic cancer. In vitro kinase assay (SIK1 phosphorylation of HDAC5), co-immunoprecipitation (14-3-3, TRIM28), STAT6 deacetylation assay, SLC7A11 promoter analysis, organoid and PDX models Cancer letters Medium 40250791

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 A novel microRNA targeting HDAC5 regulates osteoblast differentiation in mice and contributes to primary osteoporosis in humans. The Journal of clinical investigation 389 19920351
2003 Regulation of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha ) and mitochondrial function by MEF2 and HDAC5. Proceedings of the National Academy of Sciences of the United States of America 343 12578979
2013 Injury-induced HDAC5 nuclear export is essential for axon regeneration. Cell 259 24209626
2003 Neuronal activity-dependent nucleocytoplasmic shuttling of HDAC4 and HDAC5. Journal of neurochemistry 250 12641737
2012 HDAC5 is a novel injury-regulated tubulin deacetylase controlling axon regeneration. The EMBO journal 178 22692128
2000 mHDA1/HDAC5 histone deacetylase interacts with and represses MEF2A transcriptional activity. The Journal of biological chemistry 175 10748098
2021 METTL14-regulated PI3K/Akt signaling pathway via PTEN affects HDAC5-mediated epithelial-mesenchymal transition of renal tubular cells in diabetic kidney disease. Cell death & disease 174 33414476
2010 HDAC5 and HDAC9 in medulloblastoma: novel markers for risk stratification and role in tumor cell growth. Clinical cancer research : an official journal of the American Association for Cancer Research 168 20413433
2009 Fluid shear stress stimulates phosphorylation-dependent nuclear export of HDAC5 and mediates expression of KLF2 and eNOS. Blood 160 20042720
2013 Histone deacetylase (HDAC) inhibitors with a novel connecting unit linker region reveal a selectivity profile for HDAC4 and HDAC5 with improved activity against chemoresistant cancer cells. Journal of medicinal chemistry 152 23252603
2015 HDAC5 controls MEF2C-driven sclerostin expression in osteocytes. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 126 25271055
2011 Specific control of pancreatic endocrine β- and δ-cell mass by class IIa histone deacetylases HDAC4, HDAC5, and HDAC9. Diabetes 114 21953612
2015 AMPK-HDAC5 pathway facilitates nuclear accumulation of HIF-1α and functional activation of HIF-1 by deacetylating Hsp70 in the cytosol. Cell cycle (Georgetown, Tex.) 99 26061431
2017 HDAC5 and Its Target Gene, Npas4, Function in the Nucleus Accumbens to Regulate Cocaine-Conditioned Behaviors. Neuron 98 28957664
2016 Functional interaction of histone deacetylase 5 (HDAC5) and lysine-specific demethylase 1 (LSD1) promotes breast cancer progression. Oncogene 88 27212032
2014 HDAC inhibitors target HDAC5, upregulate microRNA-125a-5p, and induce apoptosis in breast cancer cells. Molecular therapy : the journal of the American Society of Gene Therapy 87 25531695
2019 Sodium butyrate attenuates angiotensin II-induced cardiac hypertrophy by inhibiting COX2/PGE2 pathway via a HDAC5/HDAC6-dependent mechanism. Journal of cellular and molecular medicine 83 31565858
2020 CD13 promotes hepatocellular carcinogenesis and sorafenib resistance by activating HDAC5-LSD1-NF-κB oncogenic signaling. Clinical and translational medicine 81 33377659
2003 Altered interaction of HDAC5 with GATA-1 during MEL cell differentiation. Oncogene 80 14668799
2006 Altered HDAC5 and CREB mRNA expressions in the peripheral leukocytes of major depression. Progress in neuro-psychopharmacology & biological psychiatry 78 17258370
2012 α2-Adrenoceptor agonist dexmedetomidine protects septic acute kidney injury through increasing BMP-7 and inhibiting HDAC2 and HDAC5. American journal of physiology. Renal physiology 77 22933299
2020 A FAK/HDAC5 signaling axis controls osteocyte mechanotransduction. Nature communications 75 32612176
2014 Inflammatory cytokines epigenetically regulate rheumatoid arthritis fibroblast-like synoviocyte activation by suppressing HDAC5 expression. Annals of the rheumatic diseases 69 25452308
2021 HDAC5 Loss Impairs RB Repression of Pro-Oncogenic Genes and Confers CDK4/6 Inhibitor Resistance in Cancer. Cancer research 68 33419772
2016 HDAC5 controls the functions of Foxp3(+) T-regulatory and CD8(+) T cells. International journal of cancer 68 26704363
2018 Neutralizing negative epigenetic regulation by HDAC5 enhances human haematopoietic stem cell homing and engraftment. Nature communications 67 30013077
2015 Ketamine produces antidepressant-like effects through phosphorylation-dependent nuclear export of histone deacetylase 5 (HDAC5) in rats. Proceedings of the National Academy of Sciences of the United States of America 65 26647181
2017 miR-124 and miR-9 mediated downregulation of HDAC5 promotes neurite development through activating MEF2C-GPM6A pathway. Journal of cellular physiology 62 28332716
2008 YY1 protects cardiac myocytes from pathologic hypertrophy by interacting with HDAC5. Molecular biology of the cell 62 18632988
2022 HDAC5 modulates PD-L1 expression and cancer immunity via p65 deacetylation in pancreatic cancer. Theranostics 60 35265200
2015 Chronic stress and antidepressant induced changes in Hdac5 and Sirt2 affect synaptic plasticity. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology 60 26433268
2018 HDAC5-LSD1 axis regulates antineoplastic effect of natural HDAC inhibitor sulforaphane in human breast cancer cells. International journal of cancer 59 29633255
2016 Both HDAC5 and HDAC6 are required for the proliferation and metastasis of melanoma cells. Journal of translational medicine 58 26747087
2014 Down-regulation of HDAC5 inhibits growth of human hepatocellular carcinoma by induction of apoptosis and cell cycle arrest. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 58 25129440
2012 HDAC5 is required for maintenance of pericentric heterochromatin, and controls cell-cycle progression and survival of human cancer cells. Cell death and differentiation 58 22301920
2019 Metformin ameliorates endotoxemia-induced endothelial pro-inflammatory responses via AMPK-dependent mediation of HDAC5 and KLF2. Biochimica et biophysica acta. Molecular basis of disease 54 31002870
2012 MEF2 is regulated by CaMKIIδ2 and a HDAC4-HDAC5 heterodimer in vascular smooth muscle cells. The Biochemical journal 53 22360269
2022 HDAC5-mediated Smad7 silencing through MEF2A is critical for fibroblast activation and hypertrophic scar formation. International journal of biological sciences 50 36263180
2017 Comprehensive immunohistochemical analysis of histone deacetylases in pancreatic neuroendocrine tumors: HDAC5 as a predictor of poor clinical outcome. Human pathology 49 28235630
2008 Inactivation of HDAC5 by SIK1 in AICAR-treated C2C12 myoblasts. Endocrine journal 48 18946175
2005 G betagamma binds histone deacetylase 5 (HDAC5) and inhibits its transcriptional co-repression activity. The Journal of biological chemistry 46 16221676
2020 Homology modeling and in silico design of novel and potential dual-acting inhibitors of human histone deacetylases HDAC5 and HDAC9 isozymes. Journal of biomolecular structure & dynamics 45 32715940
2019 PTHrP targets HDAC4 and HDAC5 to repress chondrocyte hypertrophy. JCI insight 44 30843886
2017 Hypermethylation of miRNA-589 promoter leads to upregulation of HDAC5 which promotes malignancy in non-small cell lung cancer. International journal of oncology 44 28440397
2013 HDAC5, a key component in temporal regulation of p53-mediated transactivation in response to genotoxic stress. Molecular cell 44 24120667
2022 METTL3-mediated N6-methyladenosine modification and HDAC5/YY1 promote IFFO1 downregulation in tumor development and chemo-resistance. Cancer letters 42 36257380
2017 Prior alcohol use enhances vulnerability to compulsive cocaine self-administration by promoting degradation of HDAC4 and HDAC5. Science advances 42 29109977
2006 Shuttling of HDAC5 in H9C2 cells regulates YY1 function through CaMKIV/PKD and PP2A. American journal of physiology. Cell physiology 42 16822951
2019 HDAC5-mediated deacetylation and nuclear localisation of SOX9 is critical for tamoxifen resistance in breast cancer. British journal of cancer 41 31690832
2019 HDAC5 promotes optic nerve regeneration by activating the mTOR pathway. Experimental neurology 40 30910408
2014 Compensatory regulation of HDAC5 in muscle maintains metabolic adaptive responses and metabolism in response to energetic stress. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 40 24732133
2022 Exosomal miR-9-5p derived from BMSCs alleviates apoptosis, inflammation and endoplasmic reticulum stress in spinal cord injury by regulating the HDAC5/FGF2 axis. Molecular immunology 39 35316648
2015 miR-2861 as novel HDAC5 inhibitor in CHO cells enhances productivity while maintaining product quality. Biotechnology and bioengineering 38 25997799
2014 HDAC5 promotes cell proliferation in human hepatocellular carcinoma by up-regulating Six1 expression. European review for medical and pharmacological sciences 38 24706304
2008 GLUT4 enhancer factor (GEF) interacts with MEF2A and HDAC5 to regulate the GLUT4 promoter in adipocytes. The Journal of biological chemistry 38 18216015
2008 GIT1 mediates HDAC5 activation by angiotensin II in vascular smooth muscle cells. Arteriosclerosis, thrombosis, and vascular biology 37 18292392
2011 Cocaine induces the expression of MEF2C transcription factor in rat striatum through activation of SIK1 and phosphorylation of the histone deacetylase HDAC5. Synapse (New York, N.Y.) 36 21954104
2018 Novel HDAC5-interacting motifs of Tbx3 are essential for the suppression of E-cadherin expression and for the promotion of metastasis in hepatocellular carcinoma. Signal transduction and targeted therapy 33 30151243
2017 HDAC2 and HDAC5 Up-Regulations Modulate Survivin and miR-125a-5p Expressions and Promote Hormone Therapy Resistance in Estrogen Receptor Positive Breast Cancer Cells. Frontiers in pharmacology 33 29326587
2011 Receptor-independent protein kinase C alpha (PKCalpha) signaling by calpain-generated free catalytic domains induces HDAC5 nuclear export and regulates cardiac transcription. The Journal of biological chemistry 33 21642422
2007 Molecular mechanism of transcriptional repression of AhR repressor involving ANKRA2, HDAC4, and HDAC5. Biochemical and biophysical research communications 32 17949687
2021 Insights Into the Function and Clinical Application of HDAC5 in Cancer Management. Frontiers in oncology 31 34178647
2019 HDAC5 promotes Mycoplasma pneumoniae-induced inflammation in macrophages through NF-κB activation. Life sciences 30 30738045
2017 β-Adrenergic Stimulation Induces Histone Deacetylase 5 (HDAC5) Nuclear Accumulation in Cardiomyocytes by B55α-PP2A-Mediated Dephosphorylation. Journal of the American Heart Association 30 28343149
2016 MYCN and HDAC5 transcriptionally repress CD9 to trigger invasion and metastasis in neuroblastoma. Oncotarget 29 27572323
2022 METTL3 stabilizes HDAC5 mRNA in an m6A-dependent manner to facilitate malignant proliferation of osteosarcoma cells. Cell death discovery 28 35396379
2020 Cyclic AMP represses pathological MEF2 activation by myocyte-specific hypo-phosphorylation of HDAC5. Journal of molecular and cellular cardiology 28 32485181
2014 Identification of NuRSERY, a new functional HDAC complex composed by HDAC5, GATA1, EKLF and pERK present in human erythroid cells. The international journal of biochemistry & cell biology 27 24594363
2012 NOX2-dependent ROS is required for HDAC5 nuclear efflux and contributes to HDAC4 nuclear efflux during intense repetitive activity of fast skeletal muscle fibers. American journal of physiology. Cell physiology 27 22648949
2018 Histone deacetylase 5 (HDAC5) regulates neuropathic pain through SRY-related HMG-box 10 (SOX10)-dependent mechanism in mice. Pain 26 29447134
2018 Dexmedetomidine attenuates the toxicity of β‑amyloid on neurons and astrocytes by increasing BDNF production under the regulation of HDAC2 and HDAC5. Molecular medicine reports 26 30483749
2015 HDAC5 promotes colorectal cancer cell proliferation by up-regulating DLL4 expression. International journal of clinical and experimental medicine 25 26131280
2020 Low levels of AMPK promote epithelial-mesenchymal transition in lung cancer primarily through HDAC4- and HDAC5-mediated metabolic reprogramming. Journal of cellular and molecular medicine 24 32519437
2019 β-Hydroxybutyrate, a ketone body, reduces the cytotoxic effect of cisplatin via activation of HDAC5 in human renal cortical epithelial cells. Life sciences 24 30851335
2019 Epigenetic suppression of liver X receptor β in anterior cingulate cortex by HDAC5 drives CFA-induced chronic inflammatory pain. Journal of neuroinflammation 24 31255170
2015 ERK5/HDAC5-mediated, resveratrol-, and pterostilbene-induced expression of MnSOD in human endothelial cells. Molecular nutrition & food research 24 26443543
2013 A pathway involving HDAC5, cFLIP and caspases regulates expression of the splicing regulator polypyrimidine tract binding protein in the heart. Journal of cell science 24 23424201
2022 HDAC5 Loss Enhances Phospholipid-Derived Arachidonic Acid Generation and Confers Sensitivity to cPLA2 Inhibition in Pancreatic Cancer. Cancer research 23 36102738
2020 HDAC5 inhibition reduces angiotensin II-induced vascular contraction, hypertrophy, and oxidative stress in a mouse model. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 23 33360932
2019 HDAC4 and HDAC5 form a complex with DREAM that epigenetically down-regulates NCX3 gene and its pharmacological inhibition reduces neuronal stroke damage. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 23 31696766
2015 Saponarin activates AMPK in a calcium-dependent manner and suppresses gluconeogenesis and increases glucose uptake via phosphorylation of CRTC2 and HDAC5. Bioorganic & medicinal chemistry letters 23 26471090
2013 Involvement of Epac1/Rap1/CaMKI/HDAC5 signaling cascade in the regulation of placental cell fusion. Molecular human reproduction 23 23867755
2021 Bisphenol A exposure prenatally delays bone development and bone mass accumulation in female rat offspring via the ERβ/HDAC5/TGFβ signaling pathway. Toxicology 22 34097993
2020 Fentanyl Inhibits Lung Cancer Viability and Invasion via Upregulation of miR-331-3p and Repression of HDAC5. OncoTargets and therapy 21 33380803
2018 Inflammation leads through PGE/EP3 signaling to HDAC5/MEF2-dependent transcription in cardiac myocytes. EMBO molecular medicine 21 29907596
2017 STAT3-mediated epigenetic silencing of FOXP3 in LADA T cells is regulated through HDAC5 and DNMT1. Clinical immunology (Orlando, Fla.) 21 29223407
2015 Filamin A is required in injured axons for HDAC5 activity and axon regeneration. The Journal of biological chemistry 21 26157139
2017 HDAC5 integrates ER stress and fasting signals to regulate hepatic fatty acid oxidation. Journal of lipid research 20 29229738
2015 Evidence for a non-canonical role of HDAC5 in regulation of the cardiac Ncx1 and Bnp genes. Nucleic acids research 20 26704971
2018 Deregulation of HDAC5 by Viral Interferon Regulatory Factor 3 Plays an Essential Role in Kaposi's Sarcoma-Associated Herpesvirus-Induced Lymphangiogenesis. mBio 19 29339432
2013 HDAC5 promotes osteosarcoma progression by upregulation of Twist 1 expression. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 19 24092570
2009 Alpha-adrenergic signalling activates protein kinase D and causes nuclear efflux of the transcriptional repressor HDAC5 in cultured adult mouse soleus skeletal muscle fibres. The Journal of physiology 19 19124542
2021 EGCG prevents pressure overload‑induced myocardial remodeling by downregulating overexpression of HDAC5 in mice. International journal of molecular medicine 18 34841436
2020 miR-217-regulated MEF2D-HDAC5/ND6 signaling pathway participates in the oxidative stress and inflammatory response after cerebral ischemia. Brain research 18 32311345
2021 HDAC5 promotes intestinal sepsis via the Ghrelin/E2F1/NF-κB axis. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 17 34125448
2017 PEGylated and Functionalized Aliphatic Polycarbonate Polyplex Nanoparticles for Intravenous Administration of HDAC5 siRNA in Cancer Therapy. ACS applied materials & interfaces 17 28029254
2017 Opposite effects of HDAC5 and p300 on MRTF-A-related neuronal apoptosis during ischemia/reperfusion injury in rats. Cell death & disease 17 28230854
2016 AR-42 induces apoptosis in human hepatocellular carcinoma cells via HDAC5 inhibition. Oncotarget 17 26993777
2025 SIK1 promotes ferroptosis resistance in pancreatic cancer via HDAC5-STAT6-SLC7A11 axis. Cancer letters 16 40250791
2019 HDAC5 Expression in Urothelial Carcinoma Cell Lines Inhibits Long-Term Proliferation but Can Promote Epithelial-to-Mesenchymal Transition. International journal of molecular sciences 16 31052182

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