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The protein encoded by EHMT1 is a histone methyltransferase that is part of the E2F6 complex, which represses transcription.
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EHMT1 deficiency impaired neural network activity during the transition from uncorrelated background action potential firing to synchronized network bursting. Spontaneous bursting and excitatory synaptic currents were transiently reduced, whereas miniature excitatory postsynaptic currents were not affected.
GLP (Montrer GOLGA6A Anticorps)/G9a (Montrer EHMT2 Anticorps) H3K9 methyltransferase complex is an enzyme counteracting Jmjd1a (Montrer KDM3A Anticorps)-mediated H3K9 demethylation at the Sry (Montrer SRY Anticorps) locus in gonadal somatic cells
miR (Montrer MLXIP Anticorps)-217-mediated, genetic, or pharmacological inactivation of EHMT1/2 was sufficient to promote pathological hypertrophy
EHMT1 Mediates Homeostatic Synaptic Scaling
The stress-induced Brg1 (Montrer SMARCA4 Anticorps)-G9a (Montrer EHMT2 Anticorps)/GLP (Montrer GOLGA6A Anticorps)-Dnmt3 interactions and sequence of repressive chromatin assembly on Myh6 (Montrer MYH6 Anticorps) promoter illustrates a molecular mechanism by which the heart epigenetically responds to environmental signals.
data provide genetic and pharmacologic evidence that EHMT1 and EHMT2 (Montrer EHMT2 Anticorps) are epigenetic regulators involved in gamma-globin repression and represent a novel therapeutic target for SCD (Montrer SCD Anticorps).
histone methyltransferase activities of GLP (Montrer GOLGA6A Anticorps) and G9a (Montrer EHMT2 Anticorps) are stimulated by neighboring nucleosomes that are premethylated at H3K9
Prdm16 (Montrer PRDM16 Anticorps) was required in young mice to suppress the expression of white-fat-selective genes in BAT (Montrer BAAT Anticorps) through recruitment of the histone methyltransferase Ehmt1.
G9a (Montrer EHMT2 Anticorps) and GLP (Montrer GOLGA6A Anticorps) have an essential role in normal morphogenesis of the atrioventricular septum through regulation of the size of the atrioventricular cushion.
Reduced Euchromatin histone methyltransferase 1 (Montrer DNMT1 Anticorps) causes developmental delay, hypotonia, and cranial abnormalities associated with increased bone gene expression in Kleefstra syndrome mice.
Neurodevelopmental disorders may be related to deficits in activity-dependent wiring of brain circuits during development. Although Kleefstra syndrome has been associated with dendritic and synaptic defects in mice and Drosophila, little is known about the role of EHMT1 in the development of cortical neuronal networks. We investigated the impact of EHMT1 deficiency at the network and single cell level.
These results suggest that EHMT2 (Montrer EHMT2 Anticorps) downregulation in CD4 (Montrer CD4 Anticorps)(+) T-cells may be linked to a protection mechanism against the development of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM (Montrer ATF7IP Anticorps)/TSP (Montrer THBS1 Anticorps)).
Regulated methylation and phosphorylation serve as a switch controlling G9a (Montrer EHMT2 Anticorps) and GLP (Montrer RCBTB1 Anticorps) coactivator function, suggesting that this mechanism may be a general paradigm for directing specific transcription factor and coregulator actions on different genes.
trr (Montrer TXNRD1 Anticorps) and G9a (Montrer EHMT2 Anticorps) also have common direct targets, including the Drosophila ortholog of Arc (Montrer NOL3 Anticorps) (Arc1 (Montrer CDH1 Anticorps)), a key regulator of synaptic plasticity. Our data highlight the clinical and molecular convergence between the KMT2 and EHMT protein families, which may contribute to a molecular network underlying a larger group of intellectual disability / autism spectrum disorder -related disorders.
missense variants in EHMT1 that lead to protein misfolding and disrupted histone mark binding can lead to Kleefstra Syndrome [case reports]
we find an estrogen receptor (Montrer ESR1 Anticorps)-independent synthetic lethal interaction between a GATA3 (Montrer GATA3 Anticorps) frameshift mutant with an extended C-terminus and the histone methyltransferases G9A (Montrer EHMT2 Anticorps) and GLP (Montrer RCBTB1 Anticorps), indicating perturbed epigenetic regulation
Selective degradation of the mutant EHMT1 mRNA leads to Kleefstra syndrome.
G9a (Montrer EHMT2 Anticorps) and GLP (Montrer RCBTB1 Anticorps) are required for stable maintenance of imprinted DNA methylation (Montrer HELLS Anticorps) in embryonic stem cells.
the clinical picture we found in Norwegian patients with Kleefstra syndrome is similar to the findings described in the literature. An interesting point is that in the literature >85% of the patients have a deletion of 9q34.3 and the remaining have a mutation in the EHMT1 gene, whereas in this study we found 50% with a deletion, and 50% with a mutation.
Data indicate zinc finger proteins ZNF644 (Montrer ZNF644 Anticorps) and WIZ (Montrer ZNF803 Anticorps) as two core subunits in the histone-lysine N-methyltransferase G9a (Montrer EHMT2 Anticorps)/GLP (Montrer RCBTB1 Anticorps) complex, and interact with the transcription activation domain of G9a (Montrer EHMT2 Anticorps) and GLP (Montrer RCBTB1 Anticorps).
The protein encoded by this gene is a histone methyltransferase that is part of the E2F6 complex, which represses transcription. The encoded protein methylates the Lys-9 position of histone H3, which tags it for transcriptional repression. This protein may be involved in the silencing of MYC- and E2F-responsive genes and therefore could play a role in the G0/G1 cell cycle transition. Defects in this gene are a cause of chromosome 9q subtelomeric deletion syndrome (9q-syndrome). Two transcript variants encoding different isoforms have been found for this gene.
euchromatic histone methyltransferase 1
, histone-lysine N-methyltransferase, H3 lysine-9 specific 5
, euchromatic histone-lysine N-methyltransferase 1
, histone-lysine N-methyltransferase EHMT1
, histone-lysine N-methyltransferase, H3 lysine-9 specific 5-like
, G9a-like protein 1
, lysine N-methyltransferase 1D
, G9a like protein
, H3-K9-HMTase 5
, histone H3-K9 methyltransferase 5