HCSGD entry for HMOX1
1. General information
Official gene symbol | HMOX1 |
---|---|
Entrez ID | 3162 |
Gene full name | heme oxygenase (decycling) 1 |
Other gene symbols | HMOX1D HO-1 HSP32 bK286B10 |
Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
This gene isn't in PPI subnetwork.
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
---|---|---|---|
GO:0001525 | Angiogenesis | IEA TAS | biological_process |
GO:0001666 | Response to hypoxia | IEA | biological_process |
GO:0001935 | Endothelial cell proliferation | TAS | biological_process |
GO:0002246 | Wound healing involved in inflammatory response | IMP | biological_process |
GO:0002686 | Negative regulation of leukocyte migration | TAS | biological_process |
GO:0004392 | Heme oxygenase (decyclizing) activity | IDA IEA IMP | molecular_function |
GO:0004630 | Phospholipase D activity | IEA | molecular_function |
GO:0004871 | Signal transducer activity | IMP | molecular_function |
GO:0005615 | Extracellular space | TAS | cellular_component |
GO:0005634 | Nucleus | ISS | cellular_component |
GO:0005730 | Nucleolus | IEA | cellular_component |
GO:0005783 | Endoplasmic reticulum | IDA IEA ISS | cellular_component |
GO:0005789 | Endoplasmic reticulum membrane | TAS | cellular_component |
GO:0005829 | Cytosol | IEA | cellular_component |
GO:0005901 | Caveola | IEA | cellular_component |
GO:0006778 | Porphyrin-containing compound metabolic process | TAS | biological_process |
GO:0006788 | Heme oxidation | IDA IEA | biological_process |
GO:0006879 | Cellular iron ion homeostasis | TAS | biological_process |
GO:0006979 | Response to oxidative stress | IMP | biological_process |
GO:0007264 | Small GTPase mediated signal transduction | IEA | biological_process |
GO:0007588 | Excretion | IC | biological_process |
GO:0008217 | Regulation of blood pressure | IEA | biological_process |
GO:0008219 | Cell death | ISS | biological_process |
GO:0008630 | Intrinsic apoptotic signaling pathway in response to DNA damage | IEA | biological_process |
GO:0010656 | Negative regulation of muscle cell apoptotic process | IEA | biological_process |
GO:0014806 | Smooth muscle hyperplasia | TAS | biological_process |
GO:0016020 | Membrane | TAS | cellular_component |
GO:0019899 | Enzyme binding | IEA ISS | molecular_function |
GO:0020037 | Heme binding | IDA IEA | molecular_function |
GO:0031670 | Cellular response to nutrient | IEA | biological_process |
GO:0032764 | Negative regulation of mast cell cytokine production | IEA | biological_process |
GO:0034101 | Erythrocyte homeostasis | IMP | biological_process |
GO:0034383 | Low-density lipoprotein particle clearance | TAS | biological_process |
GO:0035094 | Response to nicotine | IDA | biological_process |
GO:0035556 | Intracellular signal transduction | TAS | biological_process |
GO:0042167 | Heme catabolic process | IDA IEA TAS | biological_process |
GO:0042542 | Response to hydrogen peroxide | IEA ISS | biological_process |
GO:0042803 | Protein homodimerization activity | IDA | molecular_function |
GO:0043123 | Positive regulation of I-kappaB kinase/NF-kappaB signaling | IMP | biological_process |
GO:0043305 | Negative regulation of mast cell degranulation | IEA | biological_process |
GO:0043392 | Negative regulation of DNA binding | IEA | biological_process |
GO:0043433 | Negative regulation of sequence-specific DNA binding transcription factor activity | IEA | biological_process |
GO:0043524 | Negative regulation of neuron apoptotic process | IEA | biological_process |
GO:0043619 | Regulation of transcription from RNA polymerase II promoter in response to oxidative stress | IEA ISS | biological_process |
GO:0043627 | Response to estrogen | IEA | biological_process |
GO:0044281 | Small molecule metabolic process | TAS | biological_process |
GO:0045080 | Positive regulation of chemokine biosynthetic process | TAS | biological_process |
GO:0045765 | Regulation of angiogenesis | TAS | biological_process |
GO:0045766 | Positive regulation of angiogenesis | IEA | biological_process |
GO:0045909 | Positive regulation of vasodilation | IC | biological_process |
GO:0046872 | Metal ion binding | IEA | molecular_function |
GO:0048661 | Positive regulation of smooth muscle cell proliferation | IDA | biological_process |
GO:0048662 | Negative regulation of smooth muscle cell proliferation | IDA IEA | biological_process |
GO:0051090 | Regulation of sequence-specific DNA binding transcription factor activity | ISS | biological_process |
GO:0051260 | Protein homooligomerization | IDA | biological_process |
GO:0055072 | Iron ion homeostasis | IDA IMP | biological_process |
GO:0055085 | Transmembrane transport | TAS | biological_process |
GO:0071243 | Cellular response to arsenic-containing substance | IEA | biological_process |
GO:0071276 | Cellular response to cadmium ion | IEA | biological_process |
GO:0071456 | Cellular response to hypoxia | IEP | biological_process |
GO:1902042 | Negative regulation of extrinsic apoptotic signaling pathway via death domain receptors | IMP | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
p-value up | p-value down | FDR up | FDR down |
---|---|---|---|
0.0056185593 | 0.2384659739 | 0.1971814667 | 0.9391983989 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
Data source | Up or down | Log fold change |
---|---|---|
GSE11954 | Up | 3.0584871659 |
GSE13712_SHEAR | Down | -0.1749911347 |
GSE13712_STATIC | Up | 0.4049923211 |
GSE19018 | Down | -0.0260089270 |
GSE19899_A1 | Down | -1.0812287296 |
GSE19899_A2 | Down | -1.8487333310 |
PubMed_21979375_A1 | Up | 0.6070234193 |
PubMed_21979375_A2 | Up | 1.5221102872 |
GSE35957 | Down | -0.7938747740 |
GSE36640 | Down | -0.3311691462 |
GSE54402 | Up | 1.4549975233 |
GSE9593 | Up | 1.3893252276 |
GSE43922 | Up | 0.0017860014 |
GSE24585 | Up | 0.2912735959 |
GSE37065 | Up | 0.8110559276 |
GSE28863_A1 | Up | 0.4197152798 |
GSE28863_A2 | Up | 0.3097870405 |
GSE28863_A3 | Down | -0.4294062309 |
GSE28863_A4 | Down | -0.0102377091 |
GSE48662 | Up | 0.1088389524 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Compound | Target | Confidence score | Uniprot |
---|---|---|---|
CHEMBL536056 | CHEMBL2823 | 9 | P09601 |
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- Drugs
Name | Drug | Accession number |
---|---|---|
NADH | DB00157 | NUTR00041 | DB01907 | EXPT02287 | DB03527 |
Formic Acid | DB01942 | EXPT01461 |
Biliverdine Ix Alpha | DB02073 | EXPT00714 |
12-Phenylheme | DB02468 | EXPT00073 |
2-Phenylheme | DB03906 | EXPT00117 |
Verdoheme | DB04803 | - |
Stannsoporfin | DB04912 | - |
1-({2-[2-(4-CHLOROPHENYL)ETHYL]-1,3-DIOXOLAN-2-YL}METHYL)-1H-IMIDAZOLE | DB06914 | - |
1-(adamantan-1-yl)-2-(1H-imidazol-1-yl)ethanone | DB07342 | - |
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
---|---|---|---|---|---|
hsa-miR-16-5p | MIMAT0000069 | MIRT001455 | pSILAC//Proteomics;Other | Functional MTI (Weak) | 18668040 |
hsa-miR-196a-5p | MIMAT0000226 | MIRT004719 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 20127796 |
hsa-miR-335-5p | MIMAT0000765 | MIRT017714 | Microarray | Functional MTI (Weak) | 18185580 |
hsa-miR-148b-3p | MIMAT0000759 | MIRT019368 | Microarray | Functional MTI (Weak) | 17612493 |
hsa-miR-128-3p | MIMAT0000424 | MIRT021967 | Microarray | Functional MTI (Weak) | 17612493 |
hsa-miR-124-3p | MIMAT0000422 | MIRT022531 | Microarray | Functional MTI (Weak) | 18668037 |
hsa-miR-122-5p | MIMAT0000421 | MIRT023272 | Western blot;qRT-PCR | Functional MTI | 20633528 |
hsa-miR-122-5p | MIMAT0000421 | MIRT023272 | Microarray | Functional MTI (Weak) | 17612493 |
hsa-miR-1 | MIMAT0000416 | MIRT023697 | Proteomics | Functional MTI (Weak) | 18668040 |
hsa-miR-26b-5p | MIMAT0000083 | MIRT029307 | Microarray | Functional MTI (Weak) | 19088304 |
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- mirRecord
No target information from mirRecord
- mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 13 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
---|---|
26814705 | Furthermore, NP treatment induced the activation of Nrf2- and FOXO3A-mediated cellular stress responses, including an increased expression of heme oxygenease (HO-1), sirtuin (SIRT1), and DNA methyltransferase II (DNMT2) |
26768768 | Overexpression of HO-1 in SIRT6-null hMSCs rescued premature cellular attrition |
25175370 | Induction of heme oxygenase1 expression protects articular chondrocytes against cilostazolinduced cellular senescence |
25175370 | The aim of this study was to elucidate the mechanisms responsible for the cytoprotective effects of heme oxygenase1 (HO1) on chondrocytes in cartilage |
25175370 | Cilostazol also significantly induced HO1 expression, and the induction of HO1 expression was affected by a significant increase in reactive oxygen species (ROS) production caused by cilostazol treatment |
25175370 | Of note, pretreatment with 3morpholinosydnonimine hydrochloride (SIN1), an inducer of HO1 expression, markedly attenuated cilostazolinduced chondrocyte senescence, and thus, we examined whether HO1 directly modulates chondrocyte senescence induced by cilostazol |
25175370 | The upregulation of HO1 was found to suppress cilostazolinduced cellular senescence |
25175370 | In addition, the inhibition of HO1 activity with the iron chelator, desferrioxamine (DFO), or HO1 siRNA increased cilostazolinduced chondrocyte senescence |
25175370 | Based on these results, it can be concluded that HO1 is associated with the suppression of chondrocyte senescence, and that the enforced overexpression of HO1 protects chondrocytes against stressinduced senescence |
25050144 | Although HO-1 was upregulated in the cells of Bach1-deficient animals, the levels of ROS in Bach1-deficient HSCs were comparable to those in wild-type cells |
22539595 | In addition, exercise increased the expression of important regulators of the antioxidative defense including heme oxygenase-1 and peroxisome proliferator-activated receptor gamma coactivator 1alpha, decreased aortic reactive oxygen species levels, and prevented endothelial cell senescence in an alpha1AMPK-dependent manner |
21099244 | Additionally, depletion of BLVRA reduced the H2O2-dependent induction of heme oxygenase-1 (HO-1) in young HDFs, but not in senescent cells, suggesting an aging-dependent differential modulation of responses to oxidative stress |
20938987 | Curcumin induces heme oxygenase-1 in normal human skin fibroblasts through redox signaling: relevance for anti-aging intervention |
20938987 | METHODS AND RESULTS: Early passage young human skin fibroblasts treated with low doses of curcumin (below 20 muM) showed a time- and concentration-dependent induction of heme oxygenase-1 (HO-1), followed by compensatory increase in glutathione-S-transferase activity, GSH levels and GSH/GSSG ratio |
20938987 | The use of the antioxidant N-acetyl cysteine prevented the induction of HO-1 by curcumin |
20938987 | Pharmacological inhibition of phosphatidylinositol 3-kinase, but not other kinases, significantly prevented curcumin-induced HO-1 levels, which was corroborated by the induction of phospho-Akt levels by curcumin |
20938987 | Late passage senescent cells already had higher HO-1 levels, and further induction of HO-1 by curcumin was considerably impaired |
20448207 | Expression analysis revealed that GLP-1 can induce the oxidative defense genes HO-1 and NQO1 |
19343114 | We have also tested potential hormetins, such as curcumin and rosmarinic acid in bringing about their beneficial effects in human cells by inducing stress response pathways involving heat shock proteins and hemeoxygenase HO-1 |
18262743 | Furthermore, all three modulators tested in the present study bring about their effects by inducing stress response pathways in terms of an increase in the levels of stress proteins Hsp90, Hsp70 and heme-oxygenase-1 (HO-1), which is indicative of stress-induced hormesis bringing about the biologically beneficial effects |
16713997 | Furthermore, l-arginine-induced NO formation was accompanied by a reduction in oxidative stress and an increase in protein expression and enzyme activity of heme oxygenase (HO)-1 |
16713997 | These findings demonstrate that l-arginine prevents the onset of endothelial aging in ADMA or homocysteine-treated cells by increasing NO formation and consequently the induction of HO-1 |
16306232 | In contrast, the genes for the controlling enzymes of heme synthesis and degradation (5-aminolevulinate synthase 1 and heme oxygenase 1, respectively) were up-regulated, implying depletion of a regulatory heme pool |
11976203 | We also find that carnosine suppresses induction of heme-oxygenase-1 activity following exposure of human endothelial cells to a glycated protein |
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