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malfunction
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embryonic stem cells lacking the H3K9 HMTase G9a show a significant reduction in DNA methylation of retrotransposons, major satellite repeats and densely methylated CpG-rich promoters
malfunction
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G9a deficiency causes loss of imprinting in the placenta but not the embryo
malfunction
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knockdown of G9a or SETDB1 throughout development with an ACT5C-GAL4 driver produces organism- level defects only in the case of dSETDB1
malfunction
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lymphocyte development is unperturbed in G9a-deficient mice, G9a deficiency results in reduced usage of Iglambda L chains and a corresponding inhibition of Iglambda gene assembly in bone marrow precursors
malfunction
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inhibition of G9a/GLP in the entorhinal cortex (EC), but not in the hippocampus, enhances contextual fear conditioning relative to control animals. Downregulation of G9a/GLP activity in the EC enhances histone H3(K9) dimethylation in hippocampus area CA1, resulting in transcriptional silencing of the non-memory permissive gene COMT in the hippocampus
malfunction
an enzyme deletion mutant shows significant defects in conidiation, perithecium production and fungal virulence. Enzyme deletion results in increased tolerance to osmotic stresses and upregulated Hog1 phosphorylation
malfunction
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during oxidative stress exposure, enzyme mutants show overactivation of stress response genes, rapid depletion of glycogen, and inability to access lipid energy stores
malfunction
enzyme depletion results in embryonic lethality with severe differentiation defects in embryonic stem cells. Enzyme depletion inhibits cell proliferation in several cancer cell lines
malfunction
enzyme inhibition attenuates oncogenicity and activates the hypoxia signaling pathway
malfunction
enzyme inhibition attenuates the proliferation of HMEC-1 cells, nuclear localization of phosphorylated checkpoint kinase 1, and induces cell cycle arrest in G1 phase
malfunction
enzyme knockdown stimulates myoblast differentiation
malfunction
enzyme loss blocks germ cell differentiation
malfunction
in cultured hepatic cells, enzyme knockdown results in downregulation of insulin receptor, p-AKT and p-GSK3beta
malfunction
inhibiting the methyltransferase activity of the enzyme aggravates lipopolysaccharide-induced liver damage
malfunction
macrophage-specific enzyme-knockout mice exhibit higher serum interleukin-6 concentrations in response to lipopolysaccharide challenge and are more susceptible to endotoxin shock than wild type mice. Enzyme deficiency increases nuclear factor-kappaB p65 recruitment to the interleukin 6 promoter
malfunction
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an enzyme deletion mutant shows significant defects in conidiation, perithecium production and fungal virulence. Enzyme deletion results in increased tolerance to osmotic stresses and upregulated Hog1 phosphorylation
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physiological function
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DNA methylation of retrotransposons in embryonic stem cells requires the lysine methyltransferase G9a but not its catalytic activity
physiological function
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PRDM8 repressed the expression of steroidogenic markers, p450c17c and luteinizing hormone receptor, which indicates its regulatory role in mouse testis development and steroidogenesis
physiological function
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SETDB1 acts to maintain heterochromatin during metamorphosis, at a later stage in development than the reported action of SU(VAR)3-9, depletion of both of these enzymes has less deleterious effect than depletion of one, SETDB1 acts as a heterochromatin maintenance factor that may be required for the persistence of earlier developmental events normally governed by SU(VAR)3-9
physiological function
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G9a/GLP activity is critical for hippocampus-dependent long-term potentiation initiated in the entorhinal cortex via the perforant pathway, but not the temporoammonic pathway. G9a/GLP histone lysine dimethyltransferase complex activity in the hippocampus and the entorhinal cortex is required for gene activation and silencing during memory consolidation
physiological function
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SETDB1 is mainly responsible for mono- and trimethylation of histone H3 lysine 9 and SU (VAR)3-9 for monomethylation of histone H3 lysine 9 during spermatogenesis. Enzyme form dG9a plays no apparent role for histone H3 lysine 9 methylation during spermatogenesis and spermiogenesis
physiological function
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SUVR4 is involved in the epigenetic defense mechanism by trimethylating histone H3(K9) to suppress potentially harmful transposon activity
physiological function
SUV39H1 knockdown reduces H3K9me3 levels and impairs HCC cell growth and sphere formation. The pharmacological inhibition of SUV39H1 by chaetocin results in cell growth inhibition and inducing cellular apoptosis in culture and xenograft subcutaneous tumors. 24 of 42 HCC surgical samples display high levels of SUV39H1 expression compared with corresponding nontumor tissues. Tumor tissues show high levels of H3K9me3 and H3K9-specific methyltransferase ESET proteins in 23 (54.8%) and 29 (69.0%) samples, respectively. Expression levels of SUV39H1 but not those of ESET are significantly correlated with H3K9me3 levels
physiological function
the SET domain of isoformn Suv39 h1 is essential for repressing gene expression of BZLF1, which acts as a master regulator of the transition from latency to the lytic replication cycle in latently Epstein-Barr virus-infected cells. Depletion of Suv39 h1 protein by siRNA results in increased expression of BZLF1 mRNA in B958 cells, and Suv39 h1 inhibitor chaetocin activates BZLF1 transcription
physiological function
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the enzyme acts as a critical regulatory hub between the transcriptional and metabolic responses to oxidative stress
physiological function
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the enzyme contributes to heterochromatin formation
physiological function
the enzyme contributes to the regulation of chromatin structure
physiological function
the enzyme is a key mediator of oncogenic processes in breast cancer cells
physiological function
the enzyme is essential for full virulence of Botrytis cinerea and plays an important role in growth and development
physiological function
the enzyme is essential for the repression of developmental genes and is required during development
physiological function
the enzyme is required for cardiomyocyte homeostasis in the adult heart by mediating the repression of key genes regulating cardiomyocyte function via dimethylation of H3 lysine 9 and interaction with enhancer of zeste homolog 2, the catalytic subunit of polycomb repressive complex 2, and MEF2C-dependent gene expression by forming a complex with this transcription factor. The enzyme-MEF2C complex is required for the maintenance of heterochromatin needed for the silencing of developmental genes in the adult heart. The enzyme promotes cardiac hypertrophy by repressing antihypertrophic genes
physiological function
the enzyme modulates hepatic insulin signaling via regulating HMGA1 (high mobility group AT-hook 1, a key regulator responsible for the transcription of insulin receptor gene). In cultured hepatic cells, enzyme upregulation prevents the palmitic acid- or glucosamine-induced insulin resistance by preserving the normal level of insulin receptor and integrity of insulin signaling.
physiological function
the enzyme modulates myogenic gene expression and activation during skeletal muscle differentiation. The enzyme inhibits myoblast differentiation. The enzyme interacts with myocyte enhancer factor 2C directly and inhibits myocyte enhancer factor 2 transcription activity in a dose-dependent manner
physiological function
the enzyme plays a role in the promotion of endothelial cell proliferation
physiological function
the enzyme regulates chromatin reorganization in mouse oocytes. Maternal enzyme is vital for proper chromosome segregation in preimplantation embryos
physiological function
the enzyme regulates toll-like receptor 4-mediated inflammatory responses in macrophages. The enzyme is an epigenetic regulator of proinflammatory cytokine expression in macrophages. The enzyme suppresses transcriptional activity of interleukin 6 promoter
physiological function
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the enzyme represses E-cadherin and is associated with myometrial invasion in endometrial cancer
physiological function
Prdm3 and Prdm16 are redundant histone H3K9me1-specific methyltransferases that direct cytoplasmic H3K9me1 methylation. H3K9me1 is converted in the nucleus to H3K9me3 by the Suv39h enzyme to reinforce heterochromatin. Suv39h double null immortalized mouse embryonic fibroblasts are depleted for nuclear H3K9me3. Simultaneous depletion of Prdm3 and Prdm16 abrogates H3K9me1 methylation, prevents Suv39h-dependent H3K9me3 trimethylation, and derepresses major satellite transcription
physiological function
Drosophila melanogaster SETDB1 is an H3K9 methyltransferase and a pleiotropic regulator of the fly's development. Drosophila mutants hypomorphic or null in SETDB1 expression lose most of the H3K9 methylation as well as HP1-binding on the fourth chromosome. Binding of painting of fourth (POF), a fourth chromosome-specific protein, and the SETDB1-controlled H3K9 methylation of this chromosome are interdependent. POF and dSETDB1 interact with each other in vivo. The deregulation of H3K9 methylation, HP1-binding, and POF-binding result in a global reduction of gene expression from the fourth chromosome but not the other chromosomes. Deficiency of dSETDB1 also upregulates the expression of HP1
physiological function
female identity is secured by an H3K9me3 epigenetic pathway in which Sxl is the upstream female-specific regulator, SETDB1 is the required chromatin writer, and phf7 is one of the critical SETDB1 target genes. Germ cell specific loss of the H3K9me3 pathway members, the H3K9 methyltransferase SETDB1, WDE, and HP1a, leads to ectopic expression of genes, many of which are normally expressed in testis. SETDB1 controls the accumulation of H3K9me3 over a subset of these genes without spreading into neighboring loci
physiological function
histone H3K9 methyltransferases G9a/KMT1C, GLP/KMT1D, SETDB1/KMT1E, and Suv39h1/KMT1A, coexist in the same megacomplex. In Suv39h or G9a null cells, the remaining histone H3K9 methyltransferases are destabilized at the protein level, indicating. The four enzymes are recruited to major satellite repeats, a known Suv39h1 genomic target, but also to multiple G9a target genes. The four H3K9 histone H3K9 methyltransferases display a functional cooperation in the regulation of known G9a target genes
physiological function
knockdown of SETDB1 gene expression leads to gonocyte apoptosis and a decrease in H3K27me3, but no significant change in H3K9me3
physiological function
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the enzyme is essential for full virulence of Botrytis cinerea and plays an important role in growth and development
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