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Results 1 - 10 of 15 > >>
EC Number General Information Commentary Reference
Display the word mapDisplay the reaction diagram Show all sequences 2.1.1.366physiological function ATFa-associated factor mAM stimulates ESET enzymatic activity by increasing the Vmax and decreasing the Km. mAM facilitates the ESET-dependent conversion of dimethyl H3-K9 to the trimethyl state both in vitro and in vivo. mAM enhances ESET-mediated transcriptional repression in a SAM-dependent manner, and this repression correlates with histone H3-K9 trimethylation at the promoter 757646
Display the word mapDisplay the reaction diagram Show all sequences 2.1.1.366physiological function bivalend combinantion, dually marked histones H3K9me3/H3K14ac modification in the liver, is significantly decreased in old hepatocytes. A correlation between H3K9me3/H3K14ac bulk bivalent genomic regions and dually marked single nucleosomes is suggested. Histone H3K9 deacetylase Hdac3, as well as H3K9 methyltransferase Setdb1, found in complex Kap1, occupy both bulk and single nucleosome bivalent regions in both young and old livers, correlating to presence of H3K9me3. Expression of genes associated with bivalent regions in young liver, including those regulating cholesterol secretion and triglyceride synthesis, is upregulated in old liver once the bivalency is lost 758617
Display the word mapDisplay the reaction diagram Show all sequences 2.1.1.366physiological function deletion of Setdb1 in Meckel's cartilage tissue leads to its enlargement. Chondrocytes from the Meckel's cartilage of Setdb1 conditional KO mice show increased size. At embryonic days 16.5 and 18.5, part of the perichondrium is disrupted and mineralization is observed in the Meckel's cartilage. Inhibition of Setdb1 causes increased proliferation in chondrocytes in the Meckel's cartilage as well as in siRNA-treated ATDC5 cells. Decreased expression of chondrogenic genes, such as Sox9, Mmp13, Collagen II, and Aggrecan, is observed as a result of Setdb1 inhibition in ATDC5 cells. SMAD-dependent BMP signaling is significantly increased by the loss of Setdb1 in both the Meckel's cartilage of Setdb1 conditional KO mice and siRNA-treated ATDC5 cells 758727
Display the word mapDisplay the reaction diagram Show all sequences 2.1.1.366physiological function deletion of the catalytic domain of either histone methyltransferases EHMT2 or SETDB1 in growing oocytes leads to significant reduction of global H3K9me2 or H3K9me3 levels, respectively, in the maternal pronucleus. The asymmetry of global 5-methylcytosine (5mC) oxidation is significantly reduced in the zygotes that carry maternal mutation of either the Ehmt2 or Setdb1 genes. The levels of 5-hydroxymethylcytosine, 5-formylcytosine, and 5-carboxylcytosine increase, and 5mC levels decrease in the mutant maternal pronuclei. H3K9me3-rich rings around the nucleolar-like bodies retain 5mC in the maternal mutant zygotes. The maternal pronuclei expand in size in the mutant zygotes and contain a significantly increased number of nucleolar-like bodies compared with normal zygotes 760074
Display the word mapDisplay the reaction diagram Show all sequences 2.1.1.366physiological function embryonic stem cells exhibit high expression of the ubiquitin-conjugating enzyme UBE2K. Loss of UBE2K upregulates the trimethyltransferase SETDB1, resulting in H3K9 trimethylation and repression of neurogenic genes during differentiation 759079
Display the word mapDisplay the reaction diagram Show all sequences 2.1.1.366physiological function ESET interacts with transcription factor EST 757872
Display the word mapDisplay the reaction diagram Show all sequences 2.1.1.366physiological function H3K9 methylation reader M-phase phosphoprotein 8 (MPP8) interacts physically and functionally with SETDB1 in embryonic stem cells. MPP8 and SETDB1 coregulate a significant number of common genomic targets, especially the DNA satellite repeats 759299
Display the word mapDisplay the reaction diagram Show all sequences 2.1.1.366physiological 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 759762
Display the word mapDisplay the reaction diagram Show all sequences 2.1.1.366physiological function microRNA, miR-152-3p is involved in the regulation of SETDB1 protein levels and plays a positive regulatory role for SETDB1 expression. Inhibition of miR-152-3p results in a robust reduction in SETDB1 protein levels, though SETDB1 mRNA levels are unaffected. This is accompanied by a blockade of the biochemical pathway proceeding from H3K9me2 to H3K9me3. H3K9me2 accumulates in cells treated with an anti-miR that targets miR-152-3p. The action of a miR-152-3p mimic increases flux of the reaction leading to H3K9me3 759155
Display the word mapDisplay the reaction diagram Show all sequences 2.1.1.366physiological function Setdb1 has a constant role in endogenous retrovirus silencing. Distinctive sets of endogenous retroviruses are reactivated in different types of Setdb1-deficient somatic cells, including the VL30-class of endogenous retroviruses in mouse embryonic fibroblasts. A viral defense response is induced in immortalized Setdb1 knock-out embryonic fibroblasts 759835
Results 1 - 10 of 15 > >>