EC Number   |
Application |
Reference |
|---|
   1.14.11.68 | medicine |
demethylase Kdm6a expression is significantly upregulated in a rat acute myocardial infarction model and in hypoxia induction |
754229 |
| 1.14.11.68 | medicine |
H3K27 methylation imposes ligand-dependent regulation of the estrogen receptor alpha-dependent apoptotic response via Bcl-2 in breast cancer cells. The activation of BCL2 transcription is dependent on the simultaneous inactivation of the H3K27 methyltransferase, EZH2, and the demethylation of H3K27 at a poised enhancer by the estrogen receptor alpha-dependent recruitment of JMJD3 in hormone-dependent breast cancer cells. This pathway is modified in cells resistant to anti-estrogen, which constitutively express BCL2 |
753419 |
| 1.14.11.68 | medicine |
in renal cell carcinoma, UTX and JMJD3 transcripts are significantly increased compared to normal tissues. The level of trimethylated H3K27 is lower in cancer tissues compared to normal tissues, but expression of the H3K27 methyltransferase EZH2 is increased |
753087 |
| 1.14.11.68 | medicine |
inhibition of JMJD3 and UTX blocks reactivation-induced H3K27me3 demethylation of herpes simplex virus genomes |
754544 |
| 1.14.11.68 | medicine |
JMJD3 is upregulated in prostate cancer, and its expression is higher in metastatic prostate cancer |
753205 |
| 1.14.11.68 | medicine |
JMJD3 upregulation and NF-kappaB activation occur in the region of the wound edge during keratinocyte wound healing. JMJD3 interacts with NF-kappaB, resulting in increased expression of the inflammatory matrix metalloproteinase, and growth factor genes via demethylation of H3K27me3 at the gene promoters. Inactivation of JMJD3 or NF-kappaB results in aberrant keratinocyte wound healing |
745509 |
| 1.14.11.68 | medicine |
presence of nickel chloride upregulates the expression of H3K27me3 demethylase Jmjd3 in kidney cancer cells, which is accompanied by the reduction in the protein level of H3K27me3 |
755595 |
| 1.14.11.68 | medicine |
upon exposure of macrophages to Bacillus anthracis, lethal toxin, substantial cell death is induced with a survival rate of around 40%. The expression of Jmjd3 is induced 8fold in intoxication-resistant cells generated by treatment with lipopolysaccharides of RAW 264.7 cells. These intoxication-resistant cell lines are maintained for 8 passages and have a survival rate of around 100% on secondary exposure to lethal toxin and lipopolysaccharides |
755190 |
