EC Number   |
General Information |
Reference |
|---|
   1.14.18.B1 | malfunction |
histone demethylase JMJD3 is reduced and its target gene Snai1 expression is downregulated after HOTAIR suppression. The cell migration is inhibited in scratch test and transwell assay after HOTAIR knockdown |
745947 |
| 1.14.18.B1 | malfunction |
inactivation of JMJD3 or NF-kappaB results in aberrant keratinocyte wound healing |
745509 |
| 1.14.18.B1 | malfunction |
pharmacologic inhibition of H3K27 demethylase activity decreases the number of regenerated hair cells in response to neomycin damage. Inhibition by GSK-J4 cell causes cycle arrest and induces apoptosis in the regenerating neuromasts. Inhibition of H3K27me3 histone demethylase activity dramatically suppresses cell proliferation, activates caspase-3 levels in the regenerating neuromasts of the zebrafish lateral line, and increases the expression of p21 and p27 in neuromast cells and inhibited the ERK signaling pathway, inhibition of H3K27me3 histone demethylases by GSK-J4 significantly downregulates the phosphorylation of ERK1/2 in zebrafish |
744984 |
| 1.14.18.B1 | malfunction |
PHF8 knockout by the CRISPR-Cas9 system attenuates hypoxia signaling in 293T cells. Knockdown or knockout of PHF8 by RNAi or CRISPR-Cas9 system reduces the activation of HIF1alpha and the induction of HIF1alpha target genes including KDM3A. Despite the impaired hypoxia induced stabilization of HIF1alpha protein, the upregulation of KDM3A is only attenuated by PHF8 knockout. PHF8 knockdown elevates H3K9me2 at the 3'UTRs of KDM3A, VEGFA and at the TSS of ENO2 under normoxia. Knockdown of PHF8 increases H3K27me2 at the TSS of ENO2 and decreases H3K27me2 at the 3'UTR of ENO2, respective |
744413 |
| 1.14.18.B1 | physiological function |
H3K27 demethylases are involved in a variety of biological processes, including cell differentiation, proliferation, and cell death by regulating transcriptional activity. H3K27me3 demethylation is a key epigenetic regulator in the process of hair cell regeneration in zebrafish. The MAP kinase ERK1/2 pathway is part of the mechanism triggered by H3K27me3 inhibition to impair hair cell regeneration in zebrafish lateral line neuromasts. Specific inhibitor GSK-J4 treatment has no effect on hair cell number in the absence of neomycin damage, suggesting that H3K27 histone demethylase activity is initiated during the regeneration process to help ensure that the correct number of hair cells is regenerated |
744984 |
| 1.14.18.B1 | physiological function |
histone H3K27 demethylase JMJD3 is involved in diverse biological processes such as animal development, inflammation, senescence, and apoptosis. Histone H3K27me3 demethylase JMJD3 is involved in keratinocyte differentiation andwound healing. Enzyme 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 |
745509 |
| 1.14.18.B1 | physiological function |
JMJD3, as a histone demethylase, is capable of specifically removing the trimethyl group from the H3K27 lysine residue, triggering target gene activation. Histone demethylase JMJD3 regulates CD11a expression in lupus T cells through changes in histone H3K27 tri-methylation levels in CD4+ T cells of patients with systemic lupus erythematosus by affecting the H3K27me3 levels in the ITGAL (CD11a) promoter region. The monomethylation of H3K27 (H3K27me) is associated with gene activation, whereas H3K27me3 is associated with gene repression |
745948 |
| 1.14.18.B1 | physiological function |
long noncoding RNA HOTAIR, i.e. homeobox transcript antisense intergenic RNA, kind of non-protein coding transcripts longer than 200 nucleotides, promotes metastasis of renal cell carcinoma by upregulating histone H3K27 demethylase JMJD3. RNA HOTAIR expression is elevated in tissues of renal cell carcinoma compared to adjacent normal tissues, and positively correlates with metastasis. HOTAIR is an important promoter in metastasis of renal cell carcinoma and also plays a dual regulatory role in chromatin state by effecting both histone metylation and demethylation at different gene loci |
745947 |
| 1.14.18.B1 | physiological function |
PHF8 regulates hypoxia inducible genes mainly through sustaining the level of trimethylated histone 3 lysine 4 (H3K4me3), an active mark in transcriptional regulation. The positive role of PHF8 in hypoxia signaling extends to hypoxia-induced neuroendocrine differentiation (NED), wherein PHF8 cooperates with KDM3A to regulate the expression of NED genes. The role of PHF8 in hypoxia signaling is associated with the presence of full-length androgen receptor in CRPC cells. PHF8 is an epigenetic factor in hypoxia signaling, and the underlying regulatory mechanisms likely apply to general cancer development involving HIF1alpha. PHF8 regulates hypoxia inducible genes mainly through sustaining the level of trimethylated histone 3 lysine 4 (H3K4me3), an active mark in transcriptional regulation. PHF8 (PHD finger protein 8) is dynamically regulated during the neuroendocrine differentiation that occurs in prostate cancer, and that the c-MYC-miR-22 axis contributes to the regulation of PHF8 in the context of androgen depletion and interleukin-6 treatment. PHF8 plays a critical role in hypoxia signaling as it positively regulates KDM3A which is a critical coactivator of key transcription factor hypoxia-inducible factor 1-alpha, HIF1alpha, indirectly sustains H3K4me3 levels on select hypoxia-inducible genes, and is required for full activation of HIF1alpha through various mechanisms. In the context of prostate cancer, PHF8 appears to execute its regulatory function during hypoxia signaling in androgen receptor-positive prostate cancer cells |
744413 |
