EC Number   |
Expression |
Reference |
|---|
    4.1.1.22 | down |
both flower buds of Lonicera japonica and chlorogenic acid have inhibitory activities against the expression of 53-kDa HDC and histamine production in human epidermal keratinocytes. Chlorogenic acid shows a weaker effect on histamine production than that of flower buds of Lonicera japonica suggesting that other chemical constituents besides chlorogenic acid might contribute to the inhibitory activities. Chlorogenic acid might have an effect on the histamine production in other cells as well such as mast cells in addition to keratinocytes in the epidermis |
748712 |
| 4.1.1.22 | down |
HDC transcription is repressed by Kruppel-like factor 4 (KLF4) interacting at the level of Sp1 binding site, and by the nuclear factors Ying-yang 1 and SREBP-1a that interact with the GC box. The histone acetyl transferases KAT5 (also named as TIP60) and HDAC7 seem to be involved in this mechanisms of KLF4-mediated HDC repression acting as corepressors |
748845 |
| 4.1.1.22 | up |
12-O-tetradecanoylphorbol-13-acetate induces HDC in mast cells |
714942 |
| 4.1.1.22 | up |
histidine decarboxylase expression is 2fold higher in the B16F10 melanoma cells as compared to non-cancerous Melan-A cells |
715166 |
| 4.1.1.22 | up |
in histamine producing immune cells, HDC expression is modulated by a long list of different stimulus, including lipopolysaccharydes, polypeptides (for instance, neuropeptide P, cytokines), inflammation regulators (for instance, phorbolesters plus dexamethasone), or other compounds (for instance, the intracelular levels of polyamines). Helicobacter pylori infection promotes HDC expression through a signaling pathway involving the trans-elements Rap1 and beta-ra |
748845 |
| 4.1.1.22 | up |
induction of the histamine-forming enzyme histidine decarboxylase in skeletal muscles by prolonged muscular work, interleukin-1beta (IL-1beta) and TNF-alpha may cooperatively mediate this induction. IL-1beta increases HDC activity in all the muscles tested (masseter, pectoralis, and quadriceps femoris). HDC activity in these tissues peaks at around 5 h after the injection of IL-1beta (10 ng/g), injection of TNF-alpha (100 ng/g) also increases HDC activity in all of these muscles |
-, 747228 |
| 4.1.1.22 | up |
intravenous injection of Toll-like receptor (TLR)-4-agonistic synthetic lipid A definitely induces HDC activity in the liver, spleen, and lungs, especially the lungs, in mice (maximum activity is induced after about 3 h). The TLR2/6 agonistic synthetic diacyl-type lipopeptide FSL-1 and TLR3-agonistic poly I:C are also effective in inducing HDC, while the NOD2-agonistic synthetic muramyldipeptide (5 mg/kg) and NOD1-agonistic synthetic FK156 (D-lactyl-L-Ala-gamma-D-Glu-meso-DAP-Gly, 0.01-0.1 mg/kg), and FK565 (heptanoyl-g-D-Glu-meso-DAP-D-Ala, 0.5 mg/kg) exhibit only weak activities in this respect. Mice primed with intravenous injection of NOD1 or NOD2 agonists produce higher HDC activity following the 4-6 h later intravenous challenge with the above TLR agonists |
715168 |
| 4.1.1.22 | up |
rapid eye movement sleep deprivation (REM-SD) increases immunoreactive L-histidine decarboxylase by day 5, and it remains elevated in both dorsal and ventral aspects of the tuberomammillary complex |
-, 749082 |
| 4.1.1.22 | up |
ultraviolet B and surfactant exposure induce the expression of histamine-synthesizing enzyme histidine decarboxylase in keratinocytes. Lipopolysaccharide, house dust mite (HDM) extract, and cytokines, which are implicated in allergic inflammation, promote the expression of the enzyme and upregulate histamine levels in keratinocytes |
747438 |
| 4.1.1.22 | up |
when the cultures are supplemented with L-histidine, a 4fold increase in the HDC concentration is observed compared to the control conditions. When L-arginine is present in the medium together with histidine, the HDC concentration is only 2fold higher than the basal level |
-, 713732 |
