EC Number   |
General Information |
Reference |
|---|
   1.14.11.27 | evolution |
human JMJD2 (KDM4) H3K9 and H3K36 demethylases can be divided into members that act on both H3K9 and H3K36 and H3K9 alone, structural and phylogenetic analysis, overview. KDM4A/B/C act on both H3K9 and, less efficiently, on H3K36-methylated substrates, substrate selectivity of the human KDM4 histone demethylase subfamily, overview |
725450 |
| 1.14.11.27 | evolution |
JMJD5/KDM8 is a member of the JmjC family |
724815 |
| 1.14.11.27 | evolution |
two families of lysine demethylases (KDM) are identified. The KDM4 family consists of four members: KDM4A, KDM4B, KDM4C and KDM4D |
745919 |
| 1.14.11.27 | malfunction |
changes in RENT component recruitment at NTS regions due to loss of H3 methylases or demethylases |
744589 |
| 1.14.11.27 | malfunction |
depletion of Kdm2b/Jhdm1b in hematopoietic progenitors significantly impairs Hoxa9/Meis1-induced leukemic transformation. In leukemic stem cells, knockdown of Kdm2b/Jhdm1b impairs their self-renewing capability in vitro and in vivo |
724651 |
| 1.14.11.27 | malfunction |
dysregulated expression of KDM4A-D family promotes chromosomal instabilities |
745919 |
| 1.14.11.27 | malfunction |
dysregulated expression of KDM4A-D family promotes chromosomal instabilities. Depletion or overexpression of KDM4B does not leads to an increase in the frequency of abnormal mitotic cells and has no detectable effect on mitotic chromosome segregation |
745919 |
| 1.14.11.27 | malfunction |
dysregulated expression of KDM4A-D family promotes chromosomal instabilities. Depletion or overexpression of KDM4C, but not KDM4B, leads to over 3fold increase in the frequency of abnormal mitotic cells showing either misaligned chromosomes at metaphase, anaphase-telophase lagging chromosomes or anaphase-telophase bridges. Overexpression of a KDM4C demethylase dead mutant has no detectable effect on mitotic chromosome segregation |
745919 |
| 1.14.11.27 | malfunction |
Jhdm1a knockdown mice are still able to maintain normal glycemia, but display higher glucose production upon injection of the gluconeogenic substrate pyruvate |
-, 726260 |
| 1.14.11.27 | malfunction |
Jmjd5-/- embryos show severe growth retardation, resulting in embryonic lethality at the mid-gestation stage, Cdkn1a expression is upregulated in Jmjd5neo/neo MEFs and Jmjd5-/- embryos, which is responsible for the growth defects. phenotypes, overview. Jmjd5neo/neo hypomorphic mouse embryonic fibroblasts proliferate more slowly than wild-type |
724815 |
