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Validated All-in-One™ qPCR Primer for EHMT2(NM_006709.4) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
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. [provided by RefSeq].
Gene References into function
- interaction of G9a with a sequence-specific transcription factor that regulates gene repression through CDP/cut.
- Phe at the position equivalent to Phe(281) of Neurospora crassa DIM-5 or Phe(1205) of human G9a allows the enzyme to perform di and tri-methylation, whereas a Tyr at this position is restrictive, inhibiting tri-methylation and yielding a mono- or di-MTas
- Gfi1 associates with G9a and HDAC1 on the promoter of the cell cycle regulator p21Cip/WAF1, resulting in an increase in K9 dimethylation at histone H3
- results show human cytomegalovirus IE86 interacts with HDAC1 and histone methyltransferases G9a and Suvar(3-9)H1 and that coexpression of these chromatin remodeling enzymes with IE86 increases autorepression of the major immediate-early promoter
- Direct cooperation between DNMT1 and G9a provides a mechanism of coordinated DNA and H3K9 methylation during cell division.
- These studies establish a critical role for G9a methyltransferase, histone deacetylases, and the Swi/Snf-Brm complex in the SHP-mediated inhibition of hepatic bile acid synthesis via coordinated chromatin modification at target genes.
- ZNF200 is a novel binding partner of G9a.
- The results reveal the mechanism underlying CSB-mediated activation of ribosomal DNA transcription and link G9a-dependent histone methylation to Pol I transcription elongation through chromatin.
- These data suggest that the 2 HMTs, SUV39H1 and G9a are required to perpetuate the malignant phenotype.
- /EBPbeta as a direct substrate of G9a-mediated post-translational modification that alters the functional properties of C/EBPbeta during gene regulation.
- G9a and HP1 couple histone and DNA methylation to TNFalpha transcription silencing during endotoxin tolerance
- Chromodomain on Y-like (CDYL) is identified as a REST corepressor that physically bridges REST and the histone methylase G9a to repress transcription.
