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A cluster of genes, BAT1-BAT5, has been localized in the vicinity of the genes for TNF alpha and TNF beta. Additionally we are shipping EHMT2 Antibodies (63) and EHMT2 Kits (2) and many more products for this protein.
Showing 7 out of 7 products:
These results suggest that PIA2 modulates phyA-mediated PIF3 phosphorylation by physical interaction with PIF3 and that the secondary structure of the PIA2 N-terminus is important in this modulation.
Data indicate protein kinases FLS2 and BAK1 (show BAK1 Proteins) contribute to autoimmune signaling in ACCELERATED CELL DEATH6 (ACD6) L591F amino acid substitution.
Here we show instead that hybrid necrosis can be triggered by interactions between variants of a single gene, ACD6 (ACCELERATED CELL DEATH 6).
The effects of mutation on the structure and function of ACD6 in response to salicylic acid and disease resistance are reported.
The findings of this study suggested that G9a participates in the nerve injury-induced reduction of the Oprm1 gene likely through G9a-triggered blockage in the access of cyclic AMP response element binding protein to this gene.
GLP/G9a H3K9 methyltransferase complex is an enzyme counteracting Jmjd1a (show KDM3A Proteins)-mediated H3K9 demethylation at the Sry (show SRY Proteins) locus in gonadal somatic cells
G9a regulates cell proliferation and timing of differentiation and that G9a expression in the tooth mesenchyme is required for proper tooth development
Jmjd2c (show KDM4C Proteins) and G9a are novel enhancer-associated factors. Loss of Jmjd2c (show KDM4C Proteins) abrogates G9a recruitment and further destabilises loading of the mediator and cohesin components Med1 (show MBD4 Proteins) and Smc1a (show SMC1A Proteins) at newly activated and poised enhancers in embryonic stem cell-derived epiblast-like cells.
G9a is an important regulator in placental diseases caused by defective vascular maturation.
miR (show MLXIP Proteins)-217-mediated, genetic, or pharmacological inactivation of EHMT1 (show EHMT1 Proteins)/2 was sufficient to promote pathological hypertrophy
G9A overexpression is associated with peritoneal fibrosis.
high levels of G9a-dependent H3K9me2 at ILC3-specific genetic loci, demonstrating that G9a-mediated repression of ILC3-associated genes is critical for the optimal development of ILC2s.
G9a functions both as a co-activator and a co-repressor to enhance cellular proliferation and inhibit myogenic differentiation.
GLP, but not G9a, inhibits proteasome subunit-encoding genes expression.
G9a inhibition impairs anchorage-dependent and -independent cell growth in hepatocellular carcinoma cells
A histone H3K9-like mimic within LIG1 (show LIG1 Proteins) is methylated by G9a and GLP (show RCBTB1 Proteins) and avidly binds UHRF1 (show UHRF1 Proteins). Interaction with methylated LIG1 (show LIG1 Proteins) promotes the recruitment of UHRF1 (show UHRF1 Proteins) to DNA replication sites and is required for DNA methylation (show HELLS Proteins) maintenance.
Low G9a expression is associated with lung and colonic cancer.
G9a inhibition potentiates the anti-tumour activity of DNA double-strand break inducing agents by impairing DNA repair independent of p53 (show TP53 Proteins) status.
Inhibition of EZH2 (show EZH2 Proteins) (by GSK-343 or EPZ-6438) or inhibition of EHMT2 (by UNC-0638) in the Th17 primary cell model of HIV latency or resting memory T cells isolated from HIV-1-infected patients receiving highly active antiretroviral therapy, was sufficient to induce the reactivation of latent proviruses.
we find an estrogen receptor-independent synthetic lethal interaction between a GATA3 frameshift mutant with an extended C-terminus and the histone methyltransferases G9A and GLP, indicating perturbed epigenetic regulation
High expression of G9a and H3K9me2 in glioma tissue samples was associated with the WHO grade, which indicated that G9a and H3K9me2 may promote generation and development of glioma. BIX01294 may be a potential novel therapeutic agent in the treatment of glioma.
Depletion of G9a inhibits cell growth and induces cells apoptosis in gastric cancer.
EHMT2 inhibitor BIX-01294 is a potent inhibitor of H3K9 dimethylation and transient alterations in global histone modifications can have profound effects on embryo developmental potential.
A cluster of genes, BAT1-BAT5, has been localized in the vicinity of the genes for TNF alpha and TNF beta. This gene is found near this cluster\; it was mapped near the gene for C2 within a 120-kb region that included a HSP70 gene pair. These genes are all within the human major histocompatibility complex class III region. This gene was thought to be two different genes, NG36 and G9a, adjacent to each other but a recent publication shows that there is only a single gene. The protein encoded by this gene is thought to be involved in intracellular protein-protein interaction. There are three alternatively spliced transcript variants of this gene but only two are fully described.
ankyrin repeat-containing protein
, HLA-B associated transcript 8, rat orthologue
, euchromatic histone-lysine N-methyltransferase 2
, histone-lysine N-methyltransferase, H3 lysine-9 specific 3
, H3-K9-HMTase 3
, HLA-B associated transcript 8
, HLA-B-associated transcript 8
, histone H3-K9 methyltransferase 3
, histone-lysine N-methyltransferase EHMT2
, protein G9a
, G9A histone methyltransferase
, lysine N-methyltransferase 1C