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evolution
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Set3C is a conserved nuclear complex, Set3 interacts with Hos2
evolution
A0A0R0FIH2, A0A0R0H2W2, A0A0R0JU82, A0A0R0K0I2, I1JB12, I1JZJ1, I1K037, I1LFN1, I1LKU7, I1LTZ2, I1LWR2, I1MTD8, I1MUF8, I1MXC3, K7K0Q1, K7KKZ9, K7KL00, K7KR69 GmHDACs fall into three major groups previously named RPD3/HDA1, SIR2, and HD2, phylogenetic analysis. Chromosomal localization and duplications of HDAC genes in soybean, overview
evolution
histone deacetylase 8 (HDAC8) is a member of the class I acetyl-lysine deacetylase (HDAC) family
evolution
human histone deacetylases belong to all three known classes, class I: HDAC1, HDAC2, HDAC3, HDAC8, class II: HDAC4, HDAC5, HDAC6, HDAC7, HDAC9, HDAC10, and class III: HDAC11
evolution
the enzyme belongs to the histone deacetylase (HDAC) superfamily
evolution
the enzyme belongs to the RPD3/HDA1-like superfamily of histone deacetylases (HDACs)
evolution
the protruded arm regions are conserved among the Hda1 homologies, and residues Ile512, Ile523 and Leu525 that play key role in the domain-domain interaction are relatively conserved. The ARB2 domain of Hda1 shows structural similarity to the alpha/beta fold hydrolases
evolution
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the enzyme belongs to the histone deacetylase (HDAC) superfamily
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evolution
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the enzyme belongs to the histone deacetylase (HDAC) superfamily
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evolution
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the enzyme belongs to the histone deacetylase (HDAC) superfamily
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evolution
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the enzyme belongs to the histone deacetylase (HDAC) superfamily
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evolution
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the enzyme belongs to the histone deacetylase (HDAC) superfamily
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evolution
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the enzyme belongs to the histone deacetylase (HDAC) superfamily
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evolution
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the protruded arm regions are conserved among the Hda1 homologies, and residues Ile512, Ile523 and Leu525 that play key role in the domain-domain interaction are relatively conserved. The ARB2 domain of Hda1 shows structural similarity to the alpha/beta fold hydrolases
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evolution
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the enzyme belongs to the histone deacetylase (HDAC) superfamily
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malfunction
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alkylation (carbonylation) of conserved cysteine residues in HDAC1, -2 and -3 antagonizes their deacetylase activity and transcriptional co-repressor function
malfunction
down-regulation of HDAC gene HDA710 induces a semi-dwarf phenotype, down-regulation of HDAC gene HDA704 affects plant height and flag leaf development
malfunction
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down-regulation of HDAC gene HDA710 induces a semi-dwarf phenotype, down-regulation of HDAC gene HDA704 affects plant height and flag leaf development
malfunction
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HDAC inhibition improves DELTAF508 cystic fibrosis transmembrane conductance regulator stability and trafficking, silencing of HDAC2 and HDAC3 causes a 2.5fold and 1.5fold increase in DELTAF508 cystic fibrosis transmembrane conductance regulator mRNA, respectively, as well as an about 5fold increase in total DELTAF508 protein. Silencing of HDAC1 induces a 1.4fold stimulation of iodide efflux. In contrast, silencing of HDAC7 exhibits a 3.6fold stimulation of cAMP-mediated iodide efflux comparable to 30°C efflux
malfunction
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HDAC1 and HDAC2 with carboxy-terminal domains deleted, retain enzymatic activity but are unable to repress cartilage gene expression
malfunction
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HDAC7 knockdown causes increased nuclear beta-catenin, decreased transcription of HDAC7, decreased expression of E2F2, cyclin-D1 and cyclin-E2, and increased retinoblastoma protein
malfunction
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inhibition of histone deacetylase activity down-regulates urokinase plasminogen activator and matrix metalloproteinase-9 expression in gastric cancer
malfunction
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inhibition of SIRT1 activity leads to a recovery from the intrinsic repressive activity of orphan nuclear receptor small heterodimer partner (SHP) but not of DAX1. Inhibition of SIRT1 significantly diminishes the repressive effect of SHP on liver receptor homolog 1 transactivity. Inhibition of SIRT1 activity significantly reverses SHP-mediated inhibition of bile-acid synthesis by liver receptor homolog 1 overexpression
malfunction
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knockdown of HDAC1 can generate a remarkable defect in proliferation and also can significantly induce apoptosis and S-phase arrest in PaTu-8988 cells
malfunction
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knockdown of HDAC10 significantly increases the mRNA expression levels of thioredoxin-interacting protein and induces release of cytochrome c and activated apoptotic signaling molecules through accumulation of reactive oxygen species in SNU-620 human gastric cancer cells
malfunction
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short hairpin-RNA silencing of either HDAC2 or HDAC4 is sufficient to induce p21 expression
malfunction
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suppression of HDAC3 reduces the migration and induces the expression of E-cadherin in ovarian cancer cells
malfunction
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while brain development and adult stem cell fate are normal upon conditional deletion of HDAC2 or in mice lacking the catalytic activity of HDAC2, neurons derived from both zones of adult neurogenesis die at a specific maturation stage
malfunction
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deletion of Hos2, the catalytic subunit of the Set3 complex, produces a phenotype resembling inhibition of the Set3C by trichostatin-A
malfunction
depleting maternal isozyme HDAC2 results in hyperacetylation of H4K16, while normal deacetylation of other lysine residues of histone H3 or H4 is observed, and defective chromosome condensation and segregation during oocyte maturation occurs in a subpopulation of oocytes, leading to increased incidence of aneuploidy likely accounts for the observed sub-fertility of mice harboring Hdac2-defective oocytes. The infertility of mice harboring Hdac1-/+/Hdac2-/- oocytes is attributed to failure of those few eggs that properly mature to metaphase II to initiate DNA replication following fertilization. Hdac1-/+/Hdac2-/- eggs are fertilized but fail to initiate DNA replication. The increased amount of acetylated H4K16 likely impairs kinetochore function in oocytes lacking isozyme HDAC2 because kinetochores in mutant oocytes are less able to form coldstable microtubule attachments and less CENP-A is located at the centromere. Phenotype, overview
malfunction
hda9 and hda19 mutants show a warm-temperature-insensitive phenotype at 27°C, whereas hda15 plants displays a constitutive warm-temperature-induced phenotype at 20°C and an enhanced thermal response at 27°C. Hda9 mutation leads to differential expression of a large number of genes at 20°C and impaired induction of warm-temperature-responsive genes at 27°C. The hda15-1, hda9-1, hda9-2 and hda19 mutants display distinct hypocotyl elongation phenotypes at 20°C and 27°C under short-day conditions
malfunction
hda9 and hda19 mutants show a warm-temperature-insensitive phenotype at 27°C, whereas hda15 plants displays a constitutive warm-temperature-induced phenotype at 20°C and an enhanced thermal response at 27°C. The hda19 mutation leads to upregulation of genes mostly related to stress response at both 20°C and 27°C. The hda15-1, hda9-1, hda9-2 and hda19 mutants display distinct hypocotyl elongation phenotypes at 20°C and 27°C under short-day conditions
malfunction
histone deacetylase 7 (HDAC7) controls the thymic effector programming of natural killer T (NKT) cells, and interference with this function contributes to tissue-specific autoimmunity. Gain of HDAC7 function in thymocytes blocks both negative selection and NKT development, and diverts Va14/Ja18 TCR transgenic thymocytes into a Tconv-like lineage. Conversely, HDAC7 deletion promotes thymocyte apoptosis and causes expansion of innate-effector cells, mechanisms, overview. A mutation in HDAC7 can create problems only for specific organs in the body. In humans, mutations in HDAC7 are also associated with autoimmune disorders of the digestive tract and liver. These include inflammatory bowel diseases such as ulcerative colitis or Crohn's disease. Alteration of HDAC7 function dysregulates thymic innate effector programming and interferes with iNKT development
malfunction
histone deacetylase 7 (HDAC7) controls the thymic effector programming of natural killer T (NKT) cells, and interference with this function contributes to tissue-specific autoimmunity. Gain of HDAC7 function in thymocytes blocks both negative selection and NKT development, and diverts Va14/Ja18 TCR transgenic thymocytes into a Tconv-like lineage. Conversely, HDAC7 deletion promotes thymocyte apoptosis and causes expansion of innate-effector cells, mechanisms, overview. Alteration of HDAC7 function dysregulates thymic innate effector programming and interferes with iNKT development. While the wild-type-derived population reconstitutes hepatic iNKT cells efficiently, HDAC7-DELTAP bone marrow makes almost no contribution to this compartment in the liver, where iNKT cells are most abundant. This is also true in the thymus and spleen, demonstrating that the abnormalities observed in the intact transgenic mice are due to a cell-autonomous mechanism. Analysis of effects of loss of HDAC7 in the thymus on these phenotypes. Deletion of Hdac7 does not result in expansion of NK1.1-expressing T-cells, but significant abnormalities in the effector programming of non-tetramer-reactive thymocytes are observed
malfunction
K701 rpd3DELTA and K701 hda1DELTA alter the response to oxygen of isoamyl acetate production
malfunction
knockdown of HDT1/2 (hdt1,2i) results in an earlier switch and causes a reduced root meristem cell number. Overexpression of GA2ox2 in the RM phenocopies the hdt1,2i phenotype. Conversely, knockout of GA2ox2 partially rescues the root growth defect of hdt1,2i. The hdt1,2i-1 root tip has a gibberellin-deficient phenotype
malfunction
perturbation of the dimer interface abolishes the histone binding ability of the ARB2 domain
malfunction
RNAi-mediated HDAC1 knockdown in Gnatocerus cornutus larvae causes specific curtailment of mandibles in adults, whereas HDAC3 knockdown leads to hypertrophy. These knockdowns confer opposite effects on wing size, but little effect on the size of the core body and genital modules. PcG RNAi also reduces adult mandible size. Phenotypes, overview
malfunction
the hda15 mutation results in upregulation of many warm temperature-responsive as well as metabolic genes at 20°C and 27°C. HDA15 is associated with thermosensory mark genes at 20°C. That the association is decreased after shifting to 27°. In addition, the hda15 mutation also leads to upregulation of many metabolic genes and accumulation of primary metabolites. The hda15-1, hda9-1, hda9-2 and hda19 mutants display distinct hypocotyl elongation phenotypes at 20°C and 27°C under short-day conditions. Additive effects of the hda15-1/hfr1 double mutations on the hypocotyl and petiole lengths
malfunction
transcript levels of ILV2, ILV3 and ILV5 are elevated in Rpd3L-deficient strains (rpd3DELTA, ume1DELTA, dep1DELTA, and sds3DELTA) but not in Rpd3S-single deficient strain (rco1DELTA and eaf3DELTA) compared to wild-type K701. The transcript levels of ATF2, a minor alcohol acetyltransferase, are higher in the rpd3DELTA and ume1DELTA strains than in the parental strain. K701 rpd3DELTA and K701 hda1DELTA alter the response to oxygen of isoamyl acetate production
malfunction
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histone deacetylase 7 (HDAC7) controls the thymic effector programming of natural killer T (NKT) cells, and interference with this function contributes to tissue-specific autoimmunity. Gain of HDAC7 function in thymocytes blocks both negative selection and NKT development, and diverts Va14/Ja18 TCR transgenic thymocytes into a Tconv-like lineage. Conversely, HDAC7 deletion promotes thymocyte apoptosis and causes expansion of innate-effector cells, mechanisms, overview. Alteration of HDAC7 function dysregulates thymic innate effector programming and interferes with iNKT development. While the wild-type-derived population reconstitutes hepatic iNKT cells efficiently, HDAC7-DELTAP bone marrow makes almost no contribution to this compartment in the liver, where iNKT cells are most abundant. This is also true in the thymus and spleen, demonstrating that the abnormalities observed in the intact transgenic mice are due to a cell-autonomous mechanism. Analysis of effects of loss of HDAC7 in the thymus on these phenotypes. Deletion of Hdac7 does not result in expansion of NK1.1-expressing T-cells, but significant abnormalities in the effector programming of non-tetramer-reactive thymocytes are observed
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malfunction
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transcript levels of ILV2, ILV3 and ILV5 are elevated in Rpd3L-deficient strains (rpd3DELTA, ume1DELTA, dep1DELTA, and sds3DELTA) but not in Rpd3S-single deficient strain (rco1DELTA and eaf3DELTA) compared to wild-type K701. The transcript levels of ATF2, a minor alcohol acetyltransferase, are higher in the rpd3DELTA and ume1DELTA strains than in the parental strain. K701 rpd3DELTA and K701 hda1DELTA alter the response to oxygen of isoamyl acetate production
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malfunction
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perturbation of the dimer interface abolishes the histone binding ability of the ARB2 domain
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malfunction
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K701 rpd3DELTA and K701 hda1DELTA alter the response to oxygen of isoamyl acetate production
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malfunction
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deletion of Hos2, the catalytic subunit of the Set3 complex, produces a phenotype resembling inhibition of the Set3C by trichostatin-A
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metabolism
nitrative/oxidative stress reduce HDAC2 expression via nitration of distinct tyrosine residues. Peroxynitrite, hydrogen peroxide and cigarette smoke-conditioned medium reduce HDAC2 expression in A549 epithelial cells in vitro. This reduction is due to increased proteasomal degradation following ubiquitination rather than reduction of mRNA expression or stability
metabolism
epigenetic modifications including DNA methylation and histone post-translational modifications are closely associated with bladder cancer (BC) initiation and development, some HDACs play roles in the tumorigenicity of bladder cancer, overview. HDAC4 and HDAC9 expression is inversely correlated with Forkhead Box A1 (FOXA1), an important transcription factor in maintaining urothelial differentiation, and peroxisome proliferator-activated receptor gamma (PPARG), a steroid hormone receptor known for its oncogenic role in the development of BC
metabolism
epigenetic modifications including DNA methylation and histone post-translational modifications are closely associated with bladder cancer initiation and development, some HDACs play roles in the tumorigenicity of bladder cancer, overview
metabolism
metabolite profiling, mass spectrometric analysis
metabolism
two Arabidopsis thaliana paralogues encoding plant-specific histone deacetylases, HDT1 and HDT2, regulate a second switch from transit-amplifying cells to expanding cells
physiological function
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regulator of cellular pathways like response to stress, protein folding, microtubule stability and cell migration
physiological function
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ectopic overexpression of HDAC6 isotype increases the levels of phosphorylated epidermal growth factor receptor and phosphorylated AKT expression. HDAC6 plays an important role in the modulation of radiation response of epidermal growth factor receptor and human epidermal growth factor receptor 2-activated cells
physiological function
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HDAC catalyze the removal of acetyl groups from core histones inducing local condensation of chromatin. Therefore, HDACs are generally considered repressors of transcription. Coiled-coil domain-containing protein 6 physically interacts with HDAC1 on the amphiregulin promoter. Coiled-coil domain-containing protein 6 requires HDAC1 activity to repress cAMP responsive element binding protein 1 target gene transcription
physiological function
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HDAC1 and HDAC2 repress aggrecan and collagen 2(alpha1) expression but differ in their repression of collagen 9(alpha1), collagen 11(alpha1), dermatopontin, and cartilage oligomeric matrix protein. Carboxy-terminal domains of HDAC1 and HDAC2 are not required for enzymatic activity in vitro but are required for optimal deacetylation in vivo and repression of cartilage-specific gene expression
physiological function
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HDAC1 enhances cell proliferation of ovarian cancer cells, the expression of HDAC1 and HDAC2 is correlated with the proliferation marker Ki-67 expression, and HDAC3 stimulates cell migration with downregulation of E-cadherin in ovarian carcinoma
physiological function
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HDAC10 is involved in transcriptional downregulation of thioredoxin-interacting protein, leading to altered reactive oxygen species signaling in human gastric cancer cells
physiological function
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HDAC2 and HDAC1 are required for glucocorticoid receptor-mediated gene activation. HDAC2, however, is regulated through a different mechanism from that of HDAC1. Acetylated HDAC1 can trans-regulate HDAC2 through heterodimerization. Both HDAC1 and HDAC2 are required for mouse mammary tumor virus transcription
physiological function
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HDAC6 is necessary for protein aggregate formation and degradation
physiological function
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HDAC6 mediates TGF-beta1-induced epithelial-mesenchymal transition in A-549 cells. Splicing variant HDAC6p114 is required for TGF-beta1-activated gene expression associated with epithelial-mesenchymal transition in A-549 cells
physiological function
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HDAC7 overexpression has the ability to trump vascular endothelial growth factor signaling to inhibit endothelial cell proliferation, overexpression of HDAC7 leads to decreased nuclear beta-catenin and decreased activity of beta-catenin-dependent effectors and an associated inhibition of endothelial cell proliferation
physiological function
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HDAC7 plays a central role in restoration of DELTAF508 cystic fibrosis transmembrane conductance regulator function
physiological function
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HDACs regulate hepatocyte growth factor-induced urokinase plasminogen activator and matrix metalloproteinase-9 expression through a protein kinase C-dependent signal pathway in gastric cancer cells
physiological function
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orphan nuclear receptor small heterodimer partner (SHP) interacts and co-localizes specifically with SIRT1 in vivo. SHP recruits SIRT1 on liver receptor homolog 1 target gene promoters and SIRT1 deacetylates template-dependent histone H3 and H4 to inhibit transcription of liver receptor homolog 1 target genes
physiological function
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SIRT6 is a site-specific histone deacetylase that regulates chromatin structure. SIRT6 is implicated in fundamental biological processes in aging, including maintaining telomere integrity, fine-tuning aging-associated gene expression programs, preventing genomic instability, and maintaining metabolic homeostasis. The N-terminal extension of SIRT6 is critical for chromatin association and intrinsic catalytic activity
physiological function
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the catalytic function of HDAC2 is required in adult but not embryonic neurogenesis. HDAC2 is critically required to silence progenitor transcripts during neuronal differentiation of adult generated neurons
physiological function
the HDAC gene HDA703 is involved in histone H4 acetylation in rice, HDAC gene HDA703 has a function during plant reproductive development and seed morphology, HDA702/HDAC1 and HDA710 play a similar but important role in root and vegetative growth
physiological function
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the HDAC gene HDA703 is involved in histone H4 acetylation in rice, HDAC gene HDA703 has a function during plant reproductive development and seed morphology, HDA702/HDAC1 and HDA710 play a similar but important role in root and vegetative growth
physiological function
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the HDAC1 overexpression plays an important role in tumorigenesis of pancreatic cancer
physiological function
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activity of histone deacetylases influences splice site selection. Splicing of 700 genes in heLa cells is altered after HDAC inhibition. HDAC inhibition induces histone H4 acetylation and increases RNA Polymerase II processivity along an alternatively spliced element. In addition, HDAC inhibition reduces co-transcriptional association of the splicing regulator SRp40 with the target fibronectin exon. The depletion of HDAC1 has similar effect on fibronectin alternative splicing as global HDAC inhibition. This effect is reversed upon expression of mouse HDAC1 but not a catalytically inactive mutant
physiological function
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embryos injected with mRNA encoding a dominant-negative form of histone deacetylase lacked expression of gene Nodal related, Nr1, and exhibit randomized sidedness of the heart and viscera at stage 45. Pharmacological blockade of HDACs implicates cleavage stages as the active period. Inhibition during these early stages is correlated with an absence of Nr1 expression at stage 21, high levels of heterotaxia at stage 45, and the deposition of the epigenetic marker H3K4me2 on the Nr1 gene. The known HDAC partner protein Mad3 is a 5HT-binding regulator. While Mad3 overexpression leads to an absence of Nr1 transcription and randomizes the left-right axis, a mutant form of Mad3 lacking 5HT binding sites is not able to induce heterotaxia
physiological function
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HDAC9 gene knockdown produces dose-dependent gamma-globin gene silencing over an 80-320 nM range. Enforced expression of HDAC9 produces a dose-dependent 2.5fold increase in gammaglobin mRNA. HDAC9 binds in vivo in the upstream Ggamma-globin gene promoter region. Treatment of primary erythroid progenitors with HDAC9 siRNA results in 40 and 60% gamma-globin gene silencing in day 11 (early) and day 28 (late) progenitors, respectively. Enforced HDAC9 expression increases gamma-globin mRNA levels by 2.5fold with a simultaneous 7fold increase in fetal hemoglobin
physiological function
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in liver, class IIa HDACs HDAC4, 5, and 7, are phosphorylated and excluded from the nucleus by AMPK family kinases. In response to the fasting hormone glucagon, these HDACs are rapidly dephosphorylated and translocated to the nucleus where they associate with the promoters of gluconeogenic enzymes such as G6Pase. In turn, HDAC4/5 recruit HDAC3, which results in the acute transcriptional induction of these genes via deacetylation and activation of FOXO family transcription factors. Loss of class IIa HDACs in murine liver results in inhibition of FOXO target genes and lowers blood glucose, resulting in increased glycogen storage
physiological function
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Lysine-specific demethylase 1 has a repressive role in proinflammatory cytokine expression such as IL1alpha, IL1b,eta IL6 and IL8 and classical complement components. HDAC1 and lysine-specific demethylase 1 synergistically regulate these inflammatory-related genes
physiological function
mutation of HDA-1 by repeat-induced point mutation causes partial loss of DNA methylation. The site-specific loss of DNA methylation in hda-1 correlates with loss of H3 lysine 9 trimethylation and increased H3 acetylation. In addition, an increase in H2B acetylation is observed by two-dimensional gel electrophoresis of histones of the hda-1 mutant
physiological function
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role for Clr6 in transcriptional regulation of amino acid permease gene per1. When ammonia is used as the nitrogen source, low levels of per1 are transcribed and histones in the coding and surrounding regions of per1 are acetylated. In the presence of proline, histones at per1 are deacetylated in a Clr6-dependent manner
physiological function
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simultaneous treatment with IFNalpha2 and inhibitor trichostatin A, as well as combined HDAC1/HDAC2 silencing, restores STAT3-dependent reporter gene and endogenous gene expression, strongly suggesting that HDAC1 and HDAC2 are directly involved in repressing IFNalpha2-activated STAT3. In contrast, HDAC1 and HDAC2 activities are required for ISGF3-dependent gene expression. HDAC1 and HDAC2 differentially modulate STAT activity in response to IFNalpha2, while they are required for the induction of ISGF3-responsive genes, they impair the transcription of STAT3-dependent genes
physiological function
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Sir2 is involved in protection against Hog1-induced cell death and can suppress Hog1-induced reactive oxygen species accumulation. Therefore, cell death seems to be dictated by the balance of reactive oxygen species induced by Hog1 and the protective effect of Sir2. Prolonged activation of stress-activated protein kinase leads to cell death, by causing accumulation of reactive oxygen species. Mutations of the SCF-CDC4 ubiquitin ligase complex suppress cell death by preventing the degradation of Msn2 and Msn4 transcription factors. Accumulation of transcription factors Msn2 and Msn4 leads to the induction of PNC1, which is an activator of the Sir2 histone acetylase
physiological function
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Sirt1 inhibits T cell activation by suppressing the transcription of Bcl2-associated factor 1, Bclaf1, a protein required for T cell activation. Sirt1-null T cells have increased acetylation of the histone 3 lysine 56 residue, H3K56, at the bclaf1 promoter, as well as increasing Bclaf1 transcription. Sirt1 binds to bclaf1 promoter upon T cell receptor/CD28 stimulation by forming a complex with histone acetyltransferase p300 and NF-kappaB transcription factor Rel-A. The recruitment of Sirt1, but not p300, requires Rel-A. Knockdown of Bclaf1 suppresses the hyperactivation observed in Sirt1-/- T cells. Therefore, Sirt1 negatively regulates T cell activation via H3K56 deacetylation at the promoter region to inhibit transcription of Bclaf1
physiological function
the hda-2 mutation does not affect DNA methylation at any region tested, and the deletion and repeat-induced point mutation alleles give identical results
physiological function
the hda-3 mutation leads to global increases in histones H3 and H4 acetylation levels and to partial loss of DNA methylation
physiological function
the hda-4 mutation leads to global increases in histones H3 and H4 acetylation levels
physiological function
histone deacetylase 2 regulates chromosome segregation and kinetochore function via H4K16 deacetylation during oocyte maturation in mouse. HDAC2 is the major isozyme that regulates global histone acetylation during oocyte development and is largely responsible for the deacetylation of H4K16 during maturation. Histone deacetylation that occurs during oocyte maturation is critical for proper chromosome segregation
physiological function
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the enzyme activity promotes liver regeneration by regulating hepatocellular cell cycle progression at a step downstream of cyclin D1 induction
physiological function
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the Hos2/Set3 histone deacetylase complex (Set3C) plays a key role in the conversion of white phase to virulent opaque phase in Candida albicans. Azole resistance can be reversed by the co-administration of a histone deacetylase inhibitor, suggesting that resistance is mediated by epigenetic mechanisms possibly involving the fungal deacetylase Hos2
physiological function
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the Set3 complex acts as a repressor of hyphal differentiation and its function requires functional cAMP/PKA signaling, Set3C also controls morphogenesis through a transcription factor cluster, it is a co-factor of glycolysis and morphogenesis regulators, Set3C recruitment predicts induction and depletion predicts repression of yeast-to-hypha transition, molecular mechanism, overview. The Set3C decorates highly transcribed genes. The four phase-specific Set3C target transcription factors form a core transcriptional circuit
physiological function
Arabidopsis thaliana histone deacetylase genes HDA9, HDA15 and HDA19 play distinct roles in plant response to elevated ambient temperature. The histone deacetylases target to different sets of genes and play distinct roles in plant response to elevated ambient temperature, overview
physiological function
Arabidopsis thaliana histone deacetylase genes HDA9, HDA15 and HDA19 play distinct roles in plant response to elevated ambient temperature. The histone deacetylases target to different sets of genes and play distinct roles in plant response to elevated ambient temperature, overview. HDA15 is associated with thermosensory mark genes at 20°C. HDA15 is a direct repressor of plant thermal-responsive genes at normal temperature. HDA15 interacts with the transcription factor HFR1 (long Hypocotyl in Far Red1) to cooperatively repress warm-temperature response. HDA15 may be recruited by HFR1 to chromatin to epigenetically repress downstream target genes involved in hypocotyl elongation during plant response to low light and high temperature. HDA15 may stabilize HFR1 or enhances its function in negatively regulating PIF proteins that promote hypocotyl elongation during plant response to the growth conditions
physiological function
Arabidopsis thaliana histone deacetylase genes HDA9, HDA15 and HDA19 play distinct roles in plant response to elevated ambient temperature. The histone deacetylases target to different sets of genes and play distinct roles in plant response to elevated ambient temperature, overview. The hda9 mutation also leads to upregulation of many metabolic genes and accumulation of primary metabolites
physiological function
Hda1 is the catalytic core component of the H2B- and H3-specific histone deacetylase (HDAC) complex from Saccharomyces cerevisiae, which is involved in the epigenetic repression and plays a crucial role in transcriptional regulation and developmental events
physiological function
HDA1 might be involved in the epigenetic regulation of stress resistance genes that comprise the responses to osmotic stress and abscisic acid
physiological function
HDAC genes are non-essential in yeast, functional analysis of genes, RPD3, HDA1, SIR2, and HST1 in the Sake yeast strain Kyokai No. 701 (K701). RPD3 and Hda1 are translation regulatory proteins and histone deacetylases. Rpd3 and Hda1 may regulate isoamyl acetate production via oxygen in a Rox1-independent manner. Yeast HDACs, and maybe also HAT and their regulatory subunits, are keys to determine fermentation characteristics, and these genes may be an important target for improvement of yeast strains used for alcoholic beverage production
physiological function
HDAC genes are non-essential in yeast, functional analysis of genes, RPD3, HDA1, SIR2, and HST1 in the Sake yeast strain Kyokai No. 701 (K701). RPD3 and Hda1 are translation regulatory proteins and histone deacetylases. Rpd3L-dependent regulation of genes ILV2, ILV3 and ILV5. Rpd3 and Hda1 may regulate isoamyl acetate production via oxygen in a Rox1-independent manner. Yeast HDACs, and maybe also HAT and their regulatory subunits, are keys to determine fermentation characteristics, and these genes may be an important target for improvement of yeast strains used for alcoholic beverage production
physiological function
histone deacetylase 7 mediates tissue-specific autoimmunity via control of innate effector function in invariant natural killer T cells. HDAC7 binds transcription factor promyelocytic leukemia zinc finger protein (PLZF, ZBTB16) and modulates PLZF-dependent transcription. Autoimmune diseases are observed in HDAC7 gain-of-function in mice. Association between HDAC7 and hepatobiliary autoimmunity. Tconv development is regulated by the class IIA histone deacetylase histone deacetylase 7 (HDAC7), a TCR signal-regulated corepressor abundantly expressed in thymocytes. The activity of HDAC7 is controlled by nuclear exclusion in response to phosphorylation of conserved serine residues in their N-terminal adapter domains. HDAC7 regulates the effector programming of NKT cells in a manner that mirrors the function of PLZF. HDAC7 and PLZF inversely regulate a shared innate effector gene network that is highly relevant to autoimmune disease. HDAC7 nuclear export licenses innate effector development. HDAC7 serves as a gatekeeper of this developmental fate decision in the thymus
physiological function
histone deacetylase 7 mediates tissue-specific autoimmunity via control of innate effector function in invariant natural killer T cells. HDAC7 binds transcription factor promyelocytic leukemia zinc finger protein (PLZF, ZBTB16) and modulates PLZF-dependent transcription. HDAC7 and many of its transcriptional targets are human risk loci for IBD and PSC, autoimmune diseases that strikingly resemble the disease observed in HDAC7 gain-of-function in mice. Association between HDAC7 and hepatobiliary autoimmunity. Tconv development is regulated by the class IIA histone deacetylase histone deacetylase 7 (HDAC7), a TCR signal-regulated corepressor abundantly expressed in thymocytes. The activity of HDAC7 is controlled by nuclear exclusion in response to phosphorylation of conserved serine residues in their N-terminal adapter domains. HDAC7 regulates the effector programming of NKT cells in a manner that mirrors the function of PLZF. HDAC7 and PLZF inversely regulate a shared innate effector gene network that is highly relevant to autoimmune disease. HDAC7 nuclear export licenses innate effector development. HDAC7 serves as a gatekeeper of this developmental fate decision in the thymus
physiological function
histone deacetylases (HDACs) and polycomb group (PcG) proteins preferentially influence the size of mandibles (exaggerated male weapon) and demonstrate nutrition-dependent hypervariability in the broad-horned flour beetle, Gnatocerus cornutus. The plastic development of exaggerated traits is controlled in a module-specific manner by HDACs. The two HDACs, HDAC1 and HDAC3, appear to regulate size plasticity of mandibles and wings antagonistically, irrespective of which stage is perturbed, overview
physiological function
histone deacetylases (HDACs) and polycomb group (PcG) proteins preferentially influence the size of mandibles (exaggerated male weapon) and demonstrate nutrition-dependent hypervariability in the broad-horned flour beetle, Gnatocerus cornutus. The two HDACs, HDAC1 and HDAC3, appear to regulate size plasticity of mandibles and wings antagonistically, irrespective of which stage is perturbed, overview
physiological function
histone deacetylases (HDACs) are specifically responsible for the deacetylation of lysine residues at the N-terminal regions of the core histones (H2A, H2B, H3 and H4). In addition, HDACs may deacetylate other non-histone proteins and thus are involved in several cellular processes (e.g. differentiation, apoptosis, cancer development)
physiological function
A0A0R0FIH2, A0A0R0H2W2, A0A0R0JU82, A0A0R0K0I2, I1JB12, I1JZJ1, I1K037, I1LFN1, I1LKU7, I1LTZ2, I1LWR2, I1MTD8, I1MUF8, I1MXC3, K7K0Q1, K7KKZ9, K7KL00, K7KR69 histone deacetylases play roles in response to abiotic stresses in soybean. Histone deacetylases (HDACs) function as key epigenetic factors in repressing the expression of genes in multiple aspects of plant growth, development and plant response to abiotic or biotic stresses. Differential changes in GmHDACs transcripts accumulation occur in response to several abiotic cues, indicating that these epigenetic modifiers might potentially be part of a dynamic transcriptional response to stress in soybean. The levels of histone marks associated with plant HDACs are modulated by cold and heat in this legume
physiological function
increased expression of HDAC4 and -9 in patients with invasive squamous cell carcinoma supporting the idea that class IIa HDACs are important in the development of a basal molecular subtype and squamous differentiation in bladder cancer
physiological function
increased expression of HDAC4 and HDAC9 in patients with invasive squamous cell carcinoma supporting the idea that class IIa HDACs are important in the development of a basal molecular subtype and squamous differentiation in bladder cancer
physiological function
plant-specific histone deacetylases HDT1/2 regulate gibberellin2-oxidase2 gene expression to control Arabidopsis thaliana meristem cell number. HDT1/2 directly negatively regulate the acetylation level of the C19-gibberellin2-oxidase2 (GA2ox2) locus and repress the expression of GA2ox2 in the RM and elongation zone, transcriptome analyses. HDT1 and 2 function as part of a mechanism that modulates root growth in response to environmental factors
physiological function
the active site metal identity alters histone deacetylase 8 substrate selectivity, which may be a potential regulatory mechanism
physiological function
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histone deacetylase 7 mediates tissue-specific autoimmunity via control of innate effector function in invariant natural killer T cells. HDAC7 binds transcription factor promyelocytic leukemia zinc finger protein (PLZF, ZBTB16) and modulates PLZF-dependent transcription. Autoimmune diseases are observed in HDAC7 gain-of-function in mice. Association between HDAC7 and hepatobiliary autoimmunity. Tconv development is regulated by the class IIA histone deacetylase histone deacetylase 7 (HDAC7), a TCR signal-regulated corepressor abundantly expressed in thymocytes. The activity of HDAC7 is controlled by nuclear exclusion in response to phosphorylation of conserved serine residues in their N-terminal adapter domains. HDAC7 regulates the effector programming of NKT cells in a manner that mirrors the function of PLZF. HDAC7 and PLZF inversely regulate a shared innate effector gene network that is highly relevant to autoimmune disease. HDAC7 nuclear export licenses innate effector development. HDAC7 serves as a gatekeeper of this developmental fate decision in the thymus
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physiological function
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HDAC genes are non-essential in yeast, functional analysis of genes, RPD3, HDA1, SIR2, and HST1 in the Sake yeast strain Kyokai No. 701 (K701). RPD3 and Hda1 are translation regulatory proteins and histone deacetylases. Rpd3L-dependent regulation of genes ILV2, ILV3 and ILV5. Rpd3 and Hda1 may regulate isoamyl acetate production via oxygen in a Rox1-independent manner. Yeast HDACs, and maybe also HAT and their regulatory subunits, are keys to determine fermentation characteristics, and these genes may be an important target for improvement of yeast strains used for alcoholic beverage production
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physiological function
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Hda1 is the catalytic core component of the H2B- and H3-specific histone deacetylase (HDAC) complex from Saccharomyces cerevisiae, which is involved in the epigenetic repression and plays a crucial role in transcriptional regulation and developmental events
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physiological function
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HDAC genes are non-essential in yeast, functional analysis of genes, RPD3, HDA1, SIR2, and HST1 in the Sake yeast strain Kyokai No. 701 (K701). RPD3 and Hda1 are translation regulatory proteins and histone deacetylases. Rpd3 and Hda1 may regulate isoamyl acetate production via oxygen in a Rox1-independent manner. Yeast HDACs, and maybe also HAT and their regulatory subunits, are keys to determine fermentation characteristics, and these genes may be an important target for improvement of yeast strains used for alcoholic beverage production
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physiological function
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the Hos2/Set3 histone deacetylase complex (Set3C) plays a key role in the conversion of white phase to virulent opaque phase in Candida albicans. Azole resistance can be reversed by the co-administration of a histone deacetylase inhibitor, suggesting that resistance is mediated by epigenetic mechanisms possibly involving the fungal deacetylase Hos2
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additional information
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enzyme Hos2 is not inhibited by class I inhibitors such as MS-275
additional information
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isoform-specific regulation of zinc-dependent histone deacetylase expression, subcellular localization, and activity in regenerating liver. The signals that regulate the PH-induced metabolic response to hepatic insufficiency are not downstream, but might be upstream, of the target of suberoylanilide hydroxyamic acid's anti-regenerative activity
additional information
enzyme structure homology modelling
additional information
enzyme structure homology modelling
additional information
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enzyme structure homology modelling
additional information
similar histones substrate conversion is observed in the presence of octameric and monomeric enzyme
additional information
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similar histones substrate conversion is observed in the presence of octameric and monomeric enzyme
additional information
the ARB2 domain displays an alpha/beta sandwich architecture with an arm protruding outside. Two ARB2 domain molecules form a compact homodimer via the arm elements, and assemble as an inverse V shape. The pull-down and ITC results reveal that the ARB2 domain possesses the histone binding ability, recognizing both the H2A-H2B dimer and H3-H4 tetramer. the unique dimer architecture of the ARB2 domain coincides with the function for anchoring to histone. Hda1 consists of an N-terminal catalytic domain and a C-terminal non-catalytic domain (ARB2). The catalytic domain of Hda1 shows high sequence homology to the HDACs structures. Role of the C-terminal non-catalytic domain of Hda1 functioning in the deacetylation process, overview
additional information
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the ARB2 domain displays an alpha/beta sandwich architecture with an arm protruding outside. Two ARB2 domain molecules form a compact homodimer via the arm elements, and assemble as an inverse V shape. The pull-down and ITC results reveal that the ARB2 domain possesses the histone binding ability, recognizing both the H2A-H2B dimer and H3-H4 tetramer. the unique dimer architecture of the ARB2 domain coincides with the function for anchoring to histone. Hda1 consists of an N-terminal catalytic domain and a C-terminal non-catalytic domain (ARB2). The catalytic domain of Hda1 shows high sequence homology to the HDACs structures. Role of the C-terminal non-catalytic domain of Hda1 functioning in the deacetylation process, overview
additional information
transcript analysis of genes responsible for the production of flavor components
additional information
transcript analysis of genes responsible for the production of flavor components
additional information
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transcript analysis of genes responsible for the production of flavor components
additional information
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transcript analysis of genes responsible for the production of flavor components
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additional information
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the ARB2 domain displays an alpha/beta sandwich architecture with an arm protruding outside. Two ARB2 domain molecules form a compact homodimer via the arm elements, and assemble as an inverse V shape. The pull-down and ITC results reveal that the ARB2 domain possesses the histone binding ability, recognizing both the H2A-H2B dimer and H3-H4 tetramer. the unique dimer architecture of the ARB2 domain coincides with the function for anchoring to histone. Hda1 consists of an N-terminal catalytic domain and a C-terminal non-catalytic domain (ARB2). The catalytic domain of Hda1 shows high sequence homology to the HDACs structures. Role of the C-terminal non-catalytic domain of Hda1 functioning in the deacetylation process, overview
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additional information
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enzyme Hos2 is not inhibited by class I inhibitors such as MS-275
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