EC Number   |
Application |
Reference |
|---|
   1.14.11.66 | analysis |
KDM4A possesses the potential to act as an oxygen sensor in the context of chromatin modifications, with possible implications for epigenetic regulation in hypoxic disease states |
743916 |
| 1.14.11.66 | biotechnology |
continual removal of H3K9 promoter methylation by Jmjd2 demethylases represents a novel mechanism ensuring transcriptional competence and stability of the pluripotent cell identity |
-, 744785 |
| 1.14.11.66 | medicine |
a significant upregulation of KDM4D is observed in gastrointestinal stromal tumour tissue compared with matched normal tissue. KDM4D directly interacts with the HIF1beta gene promoter and regulates its activity, promoting tumour angiogenesis and gastrointestinal stromal tumour progression both in vitro and in vivo. KDM4D transcriptionally activates HIF1beta expression via H3K9me3 and H3K36me3 demethylation at the promoter region |
765376 |
| 1.14.11.66 | medicine |
fisetin induces DNA damage via critical transcription factor RFXAP/KDM4A-dependent histone H3K36 demethylation, thus causing inhibition of proliferation in pancreatic adenocarcinoma (PDAC). Fisetin inhibits cell proliferation and induces DNA damage and S-phase arrest in PDAC. Expression of RFXAP and other DNA-damage response genes is upregulated by fisetin. RFXAP expression is relatively low in PDAC and correlates with tumor stage and poor prognosis. Fisetin enhances the effect of chemotherapy on pancreatic cancer cells |
764436 |
| 1.14.11.66 | medicine |
histone demethylase JMJD2B is a therapeutic target in breast cancer patients |
711677 |
| 1.14.11.66 | medicine |
histone H3.3 G34R substitution mutation, found in paediatric gliomas, causes widespread changes in H3K9me3 and H3K36me3 level by interfering with the KDM4 family of K9/K36 demethylases. Expression of a targeted single-copy of H3.3 G34R at endogenous levels induces chromatin alterations that are comparable to a KDM4 A/B/C triple-knockout. H3.3 G34R preferentially binds KDM4 while simultaneously inhibiting its enzymatic activity |
765456 |
| 1.14.11.66 | medicine |
JMJD2A displays higher expression in glioma tissues than that in normal brain tissues and lower levels of H3K9me3/H3K36me3are found in glioma tissues |
764395 |
| 1.14.11.66 | medicine |
JMJD2A responds to neuropathic pain and participates in the maintenance of neuropathic pain. The mRNA and protein levels of Jmjd2a are significantly increased in the neurons of mouse undergoing neuropathic pain. Jmjd2a responds to 5-hydroxytryptamine and promotes the expression of the brain-derived neurotrophic factor (Bdnf), a protein critically involved in neuropathic pain. JMJD2A binds to the promoter of Bdnf and demethylates H3K9me3 and H3K36me3 at the Bdnf promoter to promote the expression of Bdnf. JMJD2A promotes the expression of Bdnf during neuropathic pain and neuron-specific knockout of Jmjd2a blocks the hypersensitivity of mice undergoing chronic neuropathic pain |
764639 |
| 1.14.11.66 | medicine |
JMJD2B is a feasible molecular target for anticancer therapy |
724694 |
| 1.14.11.66 | medicine |
KDM4A expression is upregulated in phosphatase and tensin homolog knockout mouse prostate tissue. Depletion of KDM4A in prostate cancer cells inhibits their proliferation and survival in vivo and vitro. Upregulation of KDM4A expression with high USP1 expression is observed in most prostate tumors and inhibition of USP1 promotes prostate cancer cells response to therapeutic agent enzalutamide |
764401 |
