EC Number |
Natural Substrates |
---|
1.14.14.18 | heme + 2 NADH + 2 H+ + 2 O2 |
NADH-dependent heme degradation system may have a biological role in regulating the concentration of respiratory hemoproteins and the disposition of the aberrant forms of the mitochondrial hemoproteins |
1.14.14.18 | heme + 2 NADPH + 2 H+ + 2 O2 |
involved in heme metabolism |
1.14.14.18 | heme + 3 AH2 + 3 O2 |
- |
1.14.14.18 | heme + 3 AH2 + 3 O2 |
requires three oxidative reaction steps, via alpha-meso-hydroxy-heme and verdoheme, detailed overview |
1.14.14.18 | heme + AH2 + O2 |
- |
1.14.14.18 | heme + AH2 + O2 |
activation of the enzyme leads to induction of the ABC transporter ABCG2, but not of ABCB6 |
1.14.14.18 | heme + AH2 + O2 |
biliverdin is involved in hemin degradation |
1.14.14.18 | heme + AH2 + O2 |
CO plays a role in cGMP production, p38 mitogen-activated protein kinase activation, and nuclear factor-kB activation, as part of the heme oxygenase-1/carbon monoxide, HO-1/CO, system, overview, correlation of HO-1-mediated cytoprotection with a decrease in intracellular free iron amounts. Biliverdin is a third generated heme catabolite by HO-1 and is converted to bilirubin by the catalytic reaction of biliverdin reductase. Both compounds are reducing species and hence may play a role in the protective response to vascular injury by oxidative stress |
1.14.14.18 | heme + AH2 + O2 |
endogenous HO-1 shows anti-apoptotic activity, and is overexpressed in various cancer diseases and might contribute to cancer progression |
1.14.14.18 | heme + AH2 + O2 |
exogenous CO activates Nrf2 through the phosphorylation of protein kinase R-like endoplasmic reticulum kinase, resulting in HO-1 expression, mechanism, overview, CO renders endothelial cells resistant to ER stress not only by downregulating C/EBP homologous protein expression via p38 mitogen-activated protein kinase activation but also by upregulating Nrf2-dependent HO-1 expression via PERK activation |