A nuclear protein critical for normal cardiovascular, nervous system, liver, spleen, and thymus development. JMJ knockout mice embryos have major heart malformations—e.g., ventricular septal defect, noncompaction of the ventricular wall, double outlet right ventricle, and dilated atria—and die soon after birth. In adult mice, JMJ is expressed at a higher level in heart, skeletal muscle, brain, and thymus. JMJ may be involved in cell growth when it is over-expressed, and may be a transcription factor.
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Especially, one TF, Jumonji, contained the CpG_2, suggesting that it may influence the CD4 gene expression through the potential binding of the predicted TFs.
Current study by Bustos and colleagues have demonstrated that JARID1B (Jumonji AT-rich interactive domain 1B) histone demethylase represses Runx2 in undifferentiated WJ-MSCs.
Indeed, glutamine supports alternative polarization by favoring Jmjd3- (jumonji domain containing -3-) dependent demethylation on the promoters of M2associated genes.
Members of the 2-ketoglutarate-dependent dioxygenase family include prolyl hydroxylase domain proteins (PHDs), ten-eleven translocation (TET) enzymes, and Jumonji C domain-containing histone lysine demethylases.
These strategies include the targeting of the histone demethylase jumonji, AT rich interactive domain 1B (JARID1B), which we found to be functionally significant in the maintenance of cancer stem cells.
Thomas, "Nitric oxide modifies global histone methylation by inhibiting Jumonji C domain-containing demethylases," Journal of Biological Chemistry, vol.
This occurs through the inhibition by D-2-hydroxyglutarate of the jumonji histone lysine demethylases (KDM) and of the TET-hydroxylases that convert 5-methylcytosine into 5-hydroxyl-methylcytosine thus leading to the accumulation of 5-methylcytosine.
Genetic knockout of the Jumonji C-domain containing protein (Jhdm2a), a H3K9 demethylase, is able to increase mice susceptibility to obesity by abnormal fat deposition and hyperlipidaemia, likely due to PPAR[alpha] expression decrease in skeletal muscles and brown fat [131].
These epigenetic regulators include such factors as histone demethylase, Jumonji D3, and microRNA let-7c.
(2) Institute of Food, Nutrition and Health, Jumonji University, 2-1-28 Sugasawa, Niiza, Saitama 3528510, Japan
[21] demonstrated that RANKL stimulation upregulated the jumonji domain-containing 3 (jmjdy) gene, and short hairpin RNAs of jmjd3 gene diminished RANKL-induced osteoclast differentiation, suggesting that JMJD3, a H3K27 demethylase, plays an important role in osteoclast differentiation.