HCSGD entry for HMOX1

1. General information

Official gene symbolHMOX1
Entrez ID3162
Gene full nameheme oxygenase (decycling) 1
Other gene symbolsHMOX1D HO-1 HSP32 bK286B10
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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This gene isn't in Literature mining network.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0001525AngiogenesisIEA TASbiological_process
GO:0001666Response to hypoxiaIEAbiological_process
GO:0001935Endothelial cell proliferationTASbiological_process
GO:0002246Wound healing involved in inflammatory responseIMPbiological_process
GO:0002686Negative regulation of leukocyte migrationTASbiological_process
GO:0004392Heme oxygenase (decyclizing) activityIDA IEA IMPmolecular_function
GO:0004630Phospholipase D activityIEAmolecular_function
GO:0004871Signal transducer activityIMPmolecular_function
GO:0005615Extracellular spaceTAScellular_component
GO:0005634NucleusISScellular_component
GO:0005730NucleolusIEAcellular_component
GO:0005783Endoplasmic reticulumIDA IEA ISScellular_component
GO:0005789Endoplasmic reticulum membraneTAScellular_component
GO:0005829CytosolIEAcellular_component
GO:0005901CaveolaIEAcellular_component
GO:0006778Porphyrin-containing compound metabolic processTASbiological_process
GO:0006788Heme oxidationIDA IEAbiological_process
GO:0006879Cellular iron ion homeostasisTASbiological_process
GO:0006979Response to oxidative stressIMPbiological_process
GO:0007264Small GTPase mediated signal transductionIEAbiological_process
GO:0007588ExcretionICbiological_process
GO:0008217Regulation of blood pressureIEAbiological_process
GO:0008219Cell deathISSbiological_process
GO:0008630Intrinsic apoptotic signaling pathway in response to DNA damageIEAbiological_process
GO:0010656Negative regulation of muscle cell apoptotic processIEAbiological_process
GO:0014806Smooth muscle hyperplasiaTASbiological_process
GO:0016020MembraneTAScellular_component
GO:0019899Enzyme bindingIEA ISSmolecular_function
GO:0020037Heme bindingIDA IEAmolecular_function
GO:0031670Cellular response to nutrientIEAbiological_process
GO:0032764Negative regulation of mast cell cytokine productionIEAbiological_process
GO:0034101Erythrocyte homeostasisIMPbiological_process
GO:0034383Low-density lipoprotein particle clearanceTASbiological_process
GO:0035094Response to nicotineIDAbiological_process
GO:0035556Intracellular signal transductionTASbiological_process
GO:0042167Heme catabolic processIDA IEA TASbiological_process
GO:0042542Response to hydrogen peroxideIEA ISSbiological_process
GO:0042803Protein homodimerization activityIDAmolecular_function
GO:0043123Positive regulation of I-kappaB kinase/NF-kappaB signalingIMPbiological_process
GO:0043305Negative regulation of mast cell degranulationIEAbiological_process
GO:0043392Negative regulation of DNA bindingIEAbiological_process
GO:0043433Negative regulation of sequence-specific DNA binding transcription factor activityIEAbiological_process
GO:0043524Negative regulation of neuron apoptotic processIEAbiological_process
GO:0043619Regulation of transcription from RNA polymerase II promoter in response to oxidative stressIEA ISSbiological_process
GO:0043627Response to estrogenIEAbiological_process
GO:0044281Small molecule metabolic processTASbiological_process
GO:0045080Positive regulation of chemokine biosynthetic processTASbiological_process
GO:0045765Regulation of angiogenesisTASbiological_process
GO:0045766Positive regulation of angiogenesisIEAbiological_process
GO:0045909Positive regulation of vasodilationICbiological_process
GO:0046872Metal ion bindingIEAmolecular_function
GO:0048661Positive regulation of smooth muscle cell proliferationIDAbiological_process
GO:0048662Negative regulation of smooth muscle cell proliferationIDA IEAbiological_process
GO:0051090Regulation of sequence-specific DNA binding transcription factor activityISSbiological_process
GO:0051260Protein homooligomerizationIDAbiological_process
GO:0055072Iron ion homeostasisIDA IMPbiological_process
GO:0055085Transmembrane transportTASbiological_process
GO:0071243Cellular response to arsenic-containing substanceIEAbiological_process
GO:0071276Cellular response to cadmium ionIEAbiological_process
GO:0071456Cellular response to hypoxiaIEPbiological_process
GO:1902042Negative regulation of extrinsic apoptotic signaling pathway via death domain receptorsIMPbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.00561855930.23846597390.19718146670.9391983989

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Up3.0584871659
GSE13712_SHEARDown-0.1749911347
GSE13712_STATICUp0.4049923211
GSE19018Down-0.0260089270
GSE19899_A1Down-1.0812287296
GSE19899_A2Down-1.8487333310
PubMed_21979375_A1Up0.6070234193
PubMed_21979375_A2Up1.5221102872
GSE35957Down-0.7938747740
GSE36640Down-0.3311691462
GSE54402Up1.4549975233
GSE9593Up1.3893252276
GSE43922Up0.0017860014
GSE24585Up0.2912735959
GSE37065Up0.8110559276
GSE28863_A1Up0.4197152798
GSE28863_A2Up0.3097870405
GSE28863_A3Down-0.4294062309
GSE28863_A4Down-0.0102377091
GSE48662Up0.1088389524

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Compound

Target

Confidence score

Uniprot

CHEMBL536056CHEMBL28239P09601
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  • Drugs

Name

Drug

Accession number

NADHDB00157 NUTR00041 | DB01907 | EXPT02287 | DB03527
Formic AcidDB01942 EXPT01461
Biliverdine Ix AlphaDB02073 EXPT00714
12-PhenylhemeDB02468 EXPT00073
2-PhenylhemeDB03906 EXPT00117
VerdohemeDB04803 -
StannsoporfinDB04912 -
1-({2-[2-(4-CHLOROPHENYL)ETHYL]-1,3-DIOXOLAN-2-YL}METHYL)-1H-IMIDAZOLEDB06914 -
1-(adamantan-1-yl)-2-(1H-imidazol-1-yl)ethanoneDB07342 -

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-16-5pMIMAT0000069MIRT001455pSILAC//Proteomics;OtherFunctional MTI (Weak)18668040
hsa-miR-196a-5pMIMAT0000226MIRT004719Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI20127796
hsa-miR-335-5pMIMAT0000765MIRT017714MicroarrayFunctional MTI (Weak)18185580
hsa-miR-148b-3pMIMAT0000759MIRT019368MicroarrayFunctional MTI (Weak)17612493
hsa-miR-128-3pMIMAT0000424MIRT021967MicroarrayFunctional MTI (Weak)17612493
hsa-miR-124-3pMIMAT0000422MIRT022531MicroarrayFunctional MTI (Weak)18668037
hsa-miR-122-5pMIMAT0000421MIRT023272Western blot;qRT-PCRFunctional MTI20633528
hsa-miR-122-5pMIMAT0000421MIRT023272MicroarrayFunctional MTI (Weak)17612493
hsa-miR-1MIMAT0000416MIRT023697ProteomicsFunctional MTI (Weak)18668040
hsa-miR-26b-5pMIMAT0000083MIRT029307MicroarrayFunctional MTI (Weak)19088304
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  • mirRecord
No target information from 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

26814705Furthermore, 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)
26768768Overexpression of HO-1 in SIRT6-null hMSCs rescued premature cellular attrition
25175370Induction of heme oxygenase1 expression protects articular chondrocytes against cilostazolinduced cellular senescence
25175370The aim of this study was to elucidate the mechanisms responsible for the cytoprotective effects of heme oxygenase1 (HO1) on chondrocytes in cartilage
25175370Cilostazol 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
25175370Of 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
25175370The upregulation of HO1 was found to suppress cilostazolinduced cellular senescence
25175370In addition, the inhibition of HO1 activity with the iron chelator, desferrioxamine (DFO), or HO1 siRNA increased cilostazolinduced chondrocyte senescence
25175370Based 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
25050144Although 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
22539595In 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
21099244Additionally, 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
20938987Curcumin induces heme oxygenase-1 in normal human skin fibroblasts through redox signaling: relevance for anti-aging intervention
20938987METHODS 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
20938987The use of the antioxidant N-acetyl cysteine prevented the induction of HO-1 by curcumin
20938987Pharmacological 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
20938987Late passage senescent cells already had higher HO-1 levels, and further induction of HO-1 by curcumin was considerably impaired
20448207Expression analysis revealed that GLP-1 can induce the oxidative defense genes HO-1 and NQO1
19343114We 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
18262743Furthermore, 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
16713997Furthermore, 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
16713997These 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
16306232In 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
11976203We 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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