Heme oxygenase, an essential enzyme in heme catabolism, cleaves heme to form biliverdin, which is subsequently converted to bilirubin by biliverdin reductase, and carbon monoxide, a putative neurotransmitter. Heme oxygenase activity is induced by its substrate heme and by various nonheme substances. Heme oxygenase occurs as 2 isozymes, an inducible heme oxygenase-1 and a constitutive heme oxygenase-2. HMOX1 and HMOX2 belong to the heme oxygenase family. [provided by RefSeq, Jul 2008]
Full Name
Heme Oxygenase 1
Function
Heme oxygenase cleaves the heme ring at the alpha methene bridge to form biliverdin. Biliverdin is subsequently converted to bilirubin by biliverdin reductase. Under physiological conditions, the activity of heme oxygenase is highest in the spleen, where senescent erythrocytes are sequestrated and destroyed. Exhibits cytoprotective effects since excess of free heme sensitizes cells to undergo apoptosis.
Biological Process
Angiogenesis Source: BHF-UCL Cell death Source: BHF-UCL Cellular iron ion homeostasis Source: CACAO Cellular response to arsenic-containing substance Source: Ensembl Cellular response to cadmium ion Source: Ensembl Cellular response to cisplatin Source: Ensembl Cellular response to heat Source: UniProtKB Cellular response to hypoxia Source: UniProtKB Cellular response to nutrient Source: Ensembl Endothelial cell proliferation Source: BHF-UCL Erythrocyte homeostasis Source: BHF-UCL Excretion Source: BHF-UCL Heme catabolic process Source: BHF-UCL Heme oxidation Source: BHF-UCL Intracellular signal transduction Source: BHF-UCL Intrinsic apoptotic signaling pathway in response to DNA damage Source: Ensembl Iron ion homeostasis Source: BHF-UCL Liver regeneration Source: Ensembl Low-density lipoprotein particle clearance Source: BHF-UCL Negative regulation of DNA binding Source: Ensembl Negative regulation of DNA-binding transcription factor activity Source: Ensembl Negative regulation of epithelial cell apoptotic process Source: Ensembl Negative regulation of extrinsic apoptotic signaling pathway via death domain receptors Source: BHF-UCL Negative regulation of leukocyte migration Source: BHF-UCL Negative regulation of macroautophagy Source: Ensembl Negative regulation of mast cell cytokine production Source: Ensembl Negative regulation of mast cell degranulation Source: Ensembl Negative regulation of muscle cell apoptotic process Source: Ensembl Negative regulation of neuron apoptotic process Source: Ensembl Negative regulation of smooth muscle cell proliferation Source: UniProtKB Negative regulation of vascular associated smooth muscle cell proliferation Source: Ensembl Positive regulation of angiogenesis Source: BHF-UCL Positive regulation of apoptotic process Source: Ensembl Positive regulation of blood vessel endothelial cell proliferation involved in sprouting angiogenesis Source: BHF-UCL Positive regulation of cell migration involved in sprouting angiogenesis Source: BHF-UCL Positive regulation of chemokine production Source: BHF-UCL Positive regulation of I-kappaB kinase/NF-kappaB signaling Source: UniProtKB Positive regulation of macroautophagy Source: Ensembl Positive regulation of smooth muscle cell proliferation Source: UniProtKB Regulation of angiogenesis Source: BHF-UCL Regulation of blood pressure Source: Ensembl Regulation of DNA-binding transcription factor activity Source: BHF-UCL Regulation of transcription from RNA polymerase II promoter in response to iron Source: Ensembl Regulation of transcription from RNA polymerase II promoter in response to oxidative stress Source: BHF-UCL Response to estrogen Source: Ensembl Response to hydrogen peroxide Source: BHF-UCL Response to nicotine Source: BHF-UCL Response to oxidative stress Source: BHF-UCL Response to xenobiotic stimulus Source: Ensembl Small GTPase mediated signal transduction Source: Ensembl Smooth muscle hyperplasia Source: BHF-UCL Wound healing involved in inflammatory response Source: BHF-UCL
Cellular Location
Microsome; Endoplasmic reticulum membrane
Involvement in disease
Heme oxygenase 1 deficiency (HMOX1D): A disease characterized by impaired stress hematopoiesis, resulting in marked erythrocyte fragmentation and intravascular hemolysis, coagulation abnormalities, endothelial damage, and iron deposition in renal and hepatic tissues. Clinical features include persistent hemolytic anemia, asplenia, nephritis, generalized erythematous rash, growth retardation and hepatomegaly.