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p(HGNC:HMOX1)

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Entity

Name
HMOX1
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 4

Oxidative stress in health and disease: The therapeutic potential of Nrf2 activation v1.0.0

Molecular chaperones and proteostasis regulation during redox imbalance v1.0.0

Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 40

a(PUBCHEM:135316034) increases p(HGNC:HMOX1) View Subject | View Object

HMOX1, induced 56-fold, encodes heme oxygenase-1, an antioxidant enzyme considered a hallmark of Nrf2 activation. PubMed:22020111

Appears in Networks:

a(PUBCHEM:135316034) increases p(HGNC:HMOX1) View Subject | View Object

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(PUBCHEM:135316034) increases p(HGNC:HMOX1) View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") increases p(HGNC:HMOX1) View Subject | View Object

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

Appears in Networks:

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:HMOX1) View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

Appears in Networks:

complex(p(HGNC:MAF), p(HGNC:NFE2L2)) increases p(HGNC:HMOX1) View Subject | View Object

Oxidative stress abrogates the Keap1-mediated degradation of Nrf2 which in turn accumulates in the nucleus where it heterodimerizes with a small musculoapo- neurotic fibrosarcoma (Maf) protein on antioxidant response elements (AREs) to stimulate the expression of a wide arrays of phase II and antioxidant enzymes including NAD(P)H quinone oxidoreductase 1 (Nqo1), heme oxygenase 1 (Hmox1), glutamane- cysteine ligase (GCL) and glutathione S transferases (GSTs) [84,85,87,88]. PubMed:24563850

Appears in Networks:

a(CHEBI:galanthamine) increases act(p(HGNC:HMOX1)) View Subject | View Object

The protective effects of galantamine in brain microvascular endothelial cells were mediated via protective gene, heme oxygenase-1 induction through NF-B activation [168] PubMed:29179999

Appears in Networks:

a(CHEBI:"desferrioxamine B") negativeCorrelation p(HGNC:HMOX1) View Subject | View Object

DFX treatment also caused a significant reduction in infiltrating CD163-positive and HO-1 positive cell in the hematoma at day 3 (Figs. 6A and B) and day 7 (Suppl Figures II & III). PubMed:27125525

Appears in Networks:
Annotations
MeSH
Cerebral Hemorrhage
Text Location
Results

a(CHEBI:"desferrioxamine B") negativeCorrelation p(HGNC:HMOX1) View Subject | View Object

Western blot analysis showed that the protein expression of HO-1 was decreased in the hematoma in the DFX treated group at day 3( HO-1/GAPDH: 0.32 ± 0.04 vs. 0.98 ± 0.07 in the vehicle-treated group, p<0.05, Fig. 6B) and day 7 (p<0.05, Suppl Figure III). PubMed:27125525

Appears in Networks:
Annotations
MeSH
Cerebral Hemorrhage
Text Location
Results

a(CHEBI:"oxidised LDL") increases p(HGNC:HMOX1) View Subject | View Object

In previous studies we found that endothelial cells exposed to oxidized LDL upregulated both heme oxygenase-1 (HO-1) and ferritin,8,9 presumably as a defense mechanism.6,11-14 PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell

a(CHEBI:"oxidised LDL") increases p(HGNC:HMOX1) View Subject | View Object

Upregulation of HO-115 and ferritin H chain16 in endothelial cells has been reported in the early phase of progression of atherosclerotic lesions. PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Atherosclerosis

deg(a(CHEBI:heme)) positiveCorrelation p(HGNC:HMOX1) View Subject | View Object

Free heme is a dangerous molecule which can be recognized and degenerated by stress-responsive enzyme oxygenase- 1 (HO-1) [16] which plays an essential role in host defense against heme. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

a(CHEBI:heme) positiveCorrelation act(p(HGNC:HMOX1)) View Subject | View Object

Lysis of red blood cells with consequent increases in free heme most likely caused the increase in HO-1 activity responsible for increased COHb concentrations, which is similar to that observed with circulatory devices [6]. PubMed:24553061

Appears in Networks:
Annotations
Text Location
Discussion

deg(a(CHEBI:heme)) positiveCorrelation p(HGNC:HMOX1) View Subject | View Object

Importantly, heme b interaction with heme oxygenase (HO; Lad et al., 2003), the enzyme responsible for heme intracellular catabolism, and hemopexin (Hx; Paoli et al., 1999), a plasmatic heme scavenger, is essential for the regulation of free heme availability and Fe recycling (Kovtunovych et al., 2010; Tolosano et al., 2010). PubMed:24904418

Appears in Networks:
Annotations
Text Location
Review

a(CHEBI:heme) increases p(HGNC:HMOX1) View Subject | View Object

Consistently, CD11b cells (granulocytes and monocytes) and iron-rich cells (macrophages) isolated from heme-treated Hx-null mice show a higher heme content and increased mRNA and protein expression of HO-1, Lferritin, and Fpn (Figure 1B-G) and elevated mRNA levels of the proinflammatory cytokine IL-6 ( Figure 1H). PubMed:26675351

Appears in Networks:
Annotations
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

a(CHEBI:heme) increases p(HGNC:HMOX1) View Subject | View Object

In agreement with the electrical cell–substrate impedance sensing data described above, the proteome changes triggered by 10 μM heme were indicative of an adaptive response with prominent induction of HMOX1 and ferritin light (FTL) and heavy (FTH1) chains (Figure 5d,left panel). PubMed:26794659

Appears in Networks:
Annotations
Cell Ontology (CL)
epithelial cell
MeSH
Kidney
Text Location
Results

a(CHEBI:heme) increases p(HGNC:HMOX1) View Subject | View Object

Despite its damaging effects, heme induces the expression of HO-1, which degrades heme to anti-inflammatory, cytoprotective, and antioxidant products [25]. PubMed:26875449

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Serum
MeSH
Malaria
Text Location
Review

a(CHEBI:heme) increases p(HGNC:HMOX1) View Subject | View Object

A recent Phase IIB clinical trial showed that preconditioning using hemin upregulated HO-1 in renal transplantation, launching further studies on clinical outcome [97]. PubMed:26875449

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Serum
MeSH
Malaria
Text Location
Review

deg(a(CHEBI:heme)) positiveCorrelation p(HGNC:HMOX1) View Subject | View Object

CD163 mediated hemoglobin/hematoma clearance is involved in the induction of HO-1, a rate-limiting enzyme for heme degradation 26. PubMed:27125525

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Cerebral Hemorrhage
Text Location
Discussion

a(CHEBI:heme) positiveCorrelation p(HGNC:HMOX1) View Subject | View Object

As predicted, HMOX1 expression levels (means 6 SD) in hemin-treated cells were much higher (7.25 6 5.02, n = 12; P , 0.001) than in nontreated controls (0.14 6 0.18, n = 9) or A1AT-treated cells (0.09 6 0.1, n = 9). PubMed:28716864

Appears in Networks:
Annotations
Cell Ontology (CL)
neutrophil
Text Location
Results

a(HM:"Atheroma lipid") increases p(HGNC:HMOX1) View Subject | View Object

At sublethal doses, atheroma lipid - whether pre-treated with heme or not - induced the expression of the stress-responsive gene HO-1, at both mRNA (Fig 3C) and protein levels (Fig 3D). PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plaque, Atherosclerotic
Text Location
Results

a(HM:erythrophagocytosis) positiveCorrelation p(HGNC:HMOX1) View Subject | View Object

A recent study, however, indicated that HO-1 is associated with blood clearance by enhancing erythrophagocytosis after stroke. PubMed:27125525

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Stroke
Text Location
Discussion

a(MESH:"Glutathione Peroxidase") decreases p(HGNC:HMOX1) View Subject | View Object

Furthermore, the induction of HO-1 was decreased (153 ± 16 versus 105 ± 3 pmol bilirubin formed per milligram of cell protein per 60 minutes, p<0.01) in endothelial cells. PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plaque, Atherosclerotic
Text Location
Results

bp(GO:"heme catabolic process") positiveCorrelation p(HGNC:HMOX1) View Subject | View Object

Once inside the cells, heme is catabolized by HO enzymes, generating equimolar amounts of biliverdin, carbon monoxide (CO), and Fe (Tenhunen et al., 1968). PubMed:24904418

Appears in Networks:
Annotations
Text Location
Review

bp(HM:"Atheromatous lesions") positiveCorrelation p(HGNC:HMOX1) View Subject | View Object

Elevated amounts of HO-1 were found in macrophages and medial smooth muscle cells of human atherosclerotic lesions.15 PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Atherosclerosis
Text Location
Discussion

complex(a(CHEBI:"carbon monoxide"), p(HGNC:HBB)) positiveCorrelation act(p(HGNC:HMOX1)) View Subject | View Object

Lysis of red blood cells with consequent increases in free heme most likely caused the increase in HO-1 activity responsible for increased COHb concentrations, which is similar to that observed with circulatory devices [6]. PubMed:24553061

Appears in Networks:
Annotations
Text Location
Discussion

p(HGNC:HBB) increases p(HGNC:HMOX1) View Subject | View Object

Immunofluorescence confirmed that renal Hb exposure triggered overexpression of HMOX1 and the unfolded protein response (UPR) chaperone HSP70 in tubule epithelial cells (Figure 2d). PubMed:26794659

Appears in Networks:
Annotations
Cell Ontology (CL)
epithelial cell
MeSH
Kidney
Text Location
Results

complex(a(CHEBI:heme), p(HGNC:ALB)) positiveCorrelation p(HGNC:HMOX1) View Subject | View Object

In endothelial cells, we found that, in the absence of serum, heme-albumin triggered a dose-dependent HMOX1 protein expression signal in an exposure range of 0–175 lmolL1. PubMed:29610666

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Mitochondria
Text Location
Results

complex(a(CHEBI:heme), a(HM:"Atheroma lipid")) increases p(HGNC:HMOX1) View Subject | View Object

Now we demonstrate that heme and hemoglobin-treated atheroma lipids also induce HO-1 in endothelial cells exposed in sublethal doses. PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Atherosclerosis
Text Location
Discussion

complex(a(CHEBI:heme), p(HGNC:ALB)) positiveCorrelation p(HGNC:HMOX1) View Subject | View Object

heme-albumin is also a robust inducer of dose-dependent HMOX1 expression in BMDMs (Figure 2D). PubMed:29610666

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Mitochondria
Text Location
Results

complex(a(CHEBI:heme), p(HGNC:ALB)) positiveCorrelation p(HGNC:HMOX1) View Subject | View Object

heme-albumin, in contrast, induced HMOX1 in a dose-dependent manner. PubMed:29610666

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Mitochondria
Text Location
Results

p(HGNC:SERPINA1) decreases p(HGNC:HMOX1) View Subject | View Object

In the presence of A1AT, hemin effect on HMOX1 expression was diminished significantly (Fig. 9A). PubMed:28716864

Appears in Networks:
Annotations
Cell Ontology (CL)
neutrophil
Text Location
Results

complex(a(HM:"Atheroma lipid"), p(HGNC:HBB)) increases p(HGNC:HMOX1) View Subject | View Object

Now we demonstrate that heme and hemoglobin-treated atheroma lipids also induce HO-1 in endothelial cells exposed in sublethal doses. PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Atherosclerosis
Text Location
Discussion

p(HGNC:CD163) increases p(HGNC:HMOX1) View Subject | View Object

CD163 mediated hemoglobin/hematoma clearance is involved in the induction of HO-1, a rate-limiting enzyme for heme degradation 26. PubMed:27125525

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Cerebral Hemorrhage
Text Location
Discussion

path(HP:atherosclerosis) negativeCorrelation p(HGNC:HMOX1) View Subject | View Object

Heme oxygenase-1, a key antioxidant enzyme that exerts cytoprotective effects in endothelial cells8,11-14 also plays an important role in preventing the development of atherosclerosis. PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Atherosclerosis
Text Location
Discussion

path(MESH:"Plaque, Atherosclerotic") negativeCorrelation p(HGNC:HMOX1) View Subject | View Object

Expression of HO-1 provides protection against atherosclerosis in several experimental models17,18 and HO-1 deficiency in humans has been associated with the appearance of vasculature fatty streaks and atheromatous plaques at age of six.19 PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Atherosclerosis

path(MESH:"Tricuspid Valve Insufficiency") negativeCorrelation p(HGNC:HMOX1) View Subject | View Object

The median values and associated interquartile ranges for hmox-1 and haptoglobin show that patients with PE+TR+ had lower expression of these genes compared with patients who were PE+TR− or PE− PubMed:26337933

Appears in Networks:
Annotations
MeSH
Pulmonary Embolism
Text Location
Results

path(MESH:"Tricuspid Valve Insufficiency") negativeCorrelation p(HGNC:HMOX1) View Subject | View Object

The inverse correlation between hmox-1 expression in circulating leukocytes and the TR jet velocity in patients with acute PE was significant (r2=0.45, p <0.001), but this significance was absent in patients without PE (r2=0.01, P=0.52). PubMed:26337933

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Pulmonary Embolism
Text Location
Results

path(MESH:Atherosclerosis) negativeCorrelation p(HGNC:HMOX1) View Subject | View Object

Expression of HO-1 provides protection against atherosclerosis in several experimental models17,18 and HO-1 deficiency in humans has been associated with the appearance of vasculature fatty streaks and atheromatous plaques at age of six.19 PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Atherosclerosis

path(MESH:Hematoma) positiveCorrelation p(HGNC:HMOX1) View Subject | View Object

HO-1 protein levels in the hematoma also increased at day-3 (HO-1/GAPDH: 0.65 ± 0.08 at day-3 vs. 0.04 ± 0.01 at 4 hour, p<0.01). PubMed:27125525

Appears in Networks:
Annotations
MeSH
Cerebral Hemorrhage
Text Location
Results

Out-Edges 31

p(HGNC:HMOX1) increases act(p(HGNC:NFE2L2)) View Subject | View Object

HMOX1, induced 56-fold, encodes heme oxygenase-1, an antioxidant enzyme considered a hallmark of Nrf2 activation. PubMed:22020111

Appears in Networks:

p(HGNC:HMOX1) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

Appears in Networks:

p(HGNC:HMOX1) positiveCorrelation bp(HM:"Atheromatous lesions") View Subject | View Object

Elevated amounts of HO-1 were found in macrophages and medial smooth muscle cells of human atherosclerotic lesions.15 PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Atherosclerosis
Text Location
Discussion

p(HGNC:HMOX1) negativeCorrelation path(MESH:Atherosclerosis) View Subject | View Object

Expression of HO-1 provides protection against atherosclerosis in several experimental models17,18 and HO-1 deficiency in humans has been associated with the appearance of vasculature fatty streaks and atheromatous plaques at age of six.19 PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Atherosclerosis

p(HGNC:HMOX1) decreases path(MESH:Atherosclerosis) View Subject | View Object

Interestingly, a 6-year-old patient with HO-1 deficiency experienced a severe atherosclerotic pathology (Yachie et al., 1999). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Cerebral Hemorrhage
Text Location
Review

p(HGNC:HMOX1) negativeCorrelation path(MESH:"Plaque, Atherosclerotic") View Subject | View Object

Expression of HO-1 provides protection against atherosclerosis in several experimental models17,18 and HO-1 deficiency in humans has been associated with the appearance of vasculature fatty streaks and atheromatous plaques at age of six.19 PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Atherosclerosis

p(HGNC:HMOX1) negativeCorrelation path(HP:atherosclerosis) View Subject | View Object

Heme oxygenase-1, a key antioxidant enzyme that exerts cytoprotective effects in endothelial cells8,11-14 also plays an important role in preventing the development of atherosclerosis. PubMed:20378845

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Atherosclerosis
Text Location
Discussion

p(HGNC:HMOX1) positiveCorrelation deg(a(CHEBI:heme)) View Subject | View Object

Free heme is a dangerous molecule which can be recognized and degenerated by stress-responsive enzyme oxygenase- 1 (HO-1) [16] which plays an essential role in host defense against heme. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

act(p(HGNC:HMOX1)) positiveCorrelation a(CHEBI:heme) View Subject | View Object

Lysis of red blood cells with consequent increases in free heme most likely caused the increase in HO-1 activity responsible for increased COHb concentrations, which is similar to that observed with circulatory devices [6]. PubMed:24553061

Appears in Networks:
Annotations
Text Location
Discussion

p(HGNC:HMOX1) positiveCorrelation deg(a(CHEBI:heme)) View Subject | View Object

Importantly, heme b interaction with heme oxygenase (HO; Lad et al., 2003), the enzyme responsible for heme intracellular catabolism, and hemopexin (Hx; Paoli et al., 1999), a plasmatic heme scavenger, is essential for the regulation of free heme availability and Fe recycling (Kovtunovych et al., 2010; Tolosano et al., 2010). PubMed:24904418

Appears in Networks:
Annotations
Text Location
Review

p(HGNC:HMOX1) increases deg(a(CHEBI:heme)) View Subject | View Object

In the extravascular compartment, cellular heme oxygenase (HO) is the most essential heme degrading protein, converting heme to free iron, biliverdin and CO [26,27]. PubMed:26368565

Appears in Networks:
Annotations
Cell Ontology (CL)
hepatocyte
MeSH
Placenta
Text Location
Introduction

p(HGNC:HMOX1) increases deg(a(CHEBI:heme)) View Subject | View Object

Despite its damaging effects, heme induces the expression of HO-1, which degrades heme to anti-inflammatory, cytoprotective, and antioxidant products [25]. PubMed:26875449

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Serum
MeSH
Malaria
Text Location
Review

p(HGNC:HMOX1) positiveCorrelation deg(a(CHEBI:heme)) View Subject | View Object

CD163 mediated hemoglobin/hematoma clearance is involved in the induction of HO-1, a rate-limiting enzyme for heme degradation 26. PubMed:27125525

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Cerebral Hemorrhage
Text Location
Discussion

p(HGNC:HMOX1) positiveCorrelation a(CHEBI:heme) View Subject | View Object

As predicted, HMOX1 expression levels (means 6 SD) in hemin-treated cells were much higher (7.25 6 5.02, n = 12; P , 0.001) than in nontreated controls (0.14 6 0.18, n = 9) or A1AT-treated cells (0.09 6 0.1, n = 9). PubMed:28716864

Appears in Networks:
Annotations
Cell Ontology (CL)
neutrophil
Text Location
Results

p(HGNC:HMOX1) increases deg(a(CHEBI:heme)) View Subject | View Object

Upon degradation of RBCs in the erythrophagosome, heme is imported into the cytoplasm for degradation by the heme-degrading enzyme heme oxygenase-1 (HMOX1) [7]. PubMed:30248094

Appears in Networks:
Annotations
MeSH
Cytoplasm
Text Location
Introduction

p(HGNC:HMOX1) increases deg(a(CHEBI:heme)) View Subject | View Object

A major intracellular antioxidant is heme oxygenase-1 (HO-1) which, through its heme-degrading activity, plays a critical role in the protection of cells. PubMed:30505280

Appears in Networks:
Annotations
MeSH
Knee
MeSH
Osteoarthritis, Knee
Text Location
Introduction

act(p(HGNC:HMOX1)) positiveCorrelation complex(a(CHEBI:"carbon monoxide"), p(HGNC:HBB)) View Subject | View Object

Lysis of red blood cells with consequent increases in free heme most likely caused the increase in HO-1 activity responsible for increased COHb concentrations, which is similar to that observed with circulatory devices [6]. PubMed:24553061

Appears in Networks:
Annotations
Text Location
Discussion

p(HGNC:HMOX1) positiveCorrelation bp(GO:"heme catabolic process") View Subject | View Object

Once inside the cells, heme is catabolized by HO enzymes, generating equimolar amounts of biliverdin, carbon monoxide (CO), and Fe (Tenhunen et al., 1968). PubMed:24904418

Appears in Networks:
Annotations
Text Location
Review

p(HGNC:HMOX1) decreases a(MESH:"Cell Adhesion Molecules") View Subject | View Object

During the resolution phase of inflammation HO-1 expression in leukocytes reduces adhesion molecules expression and leukocytes migration, thus contributing to wound healing (Wagener et al., 2003a). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

p(HGNC:HMOX1) decreases bp(GO:"leukocyte migration") View Subject | View Object

During the resolution phase of inflammation HO-1 expression in leukocytes reduces adhesion molecules expression and leukocytes migration, thus contributing to wound healing (Wagener et al., 2003a). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

p(HGNC:HMOX1) increases bp(MESH:"Wound Healing") View Subject | View Object

During the resolution phase of inflammation HO-1 expression in leukocytes reduces adhesion molecules expression and leukocytes migration, thus contributing to wound healing (Wagener et al., 2003a). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

p(HGNC:HMOX1) decreases bp(GO:"necroptotic process") View Subject | View Object

Moreover, HO-1 has a protective effect during heme-induced necroptosis. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

p(HGNC:HMOX1) negativeCorrelation path(MESH:"Tricuspid Valve Insufficiency") View Subject | View Object

The median values and associated interquartile ranges for hmox-1 and haptoglobin show that patients with PE+TR+ had lower expression of these genes compared with patients who were PE+TR− or PE− PubMed:26337933

Appears in Networks:
Annotations
MeSH
Pulmonary Embolism
Text Location
Results

p(HGNC:HMOX1) negativeCorrelation path(MESH:"Tricuspid Valve Insufficiency") View Subject | View Object

The inverse correlation between hmox-1 expression in circulating leukocytes and the TR jet velocity in patients with acute PE was significant (r2=0.45, p <0.001), but this significance was absent in patients without PE (r2=0.01, P=0.52). PubMed:26337933

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Pulmonary Embolism
Text Location
Results

p(HGNC:HMOX1) positiveCorrelation path(MESH:Hematoma) View Subject | View Object

HO-1 protein levels in the hematoma also increased at day-3 (HO-1/GAPDH: 0.65 ± 0.08 at day-3 vs. 0.04 ± 0.01 at 4 hour, p<0.01). PubMed:27125525

Appears in Networks:
Annotations
MeSH
Cerebral Hemorrhage
Text Location
Results

p(HGNC:HMOX1) negativeCorrelation a(CHEBI:"desferrioxamine B") View Subject | View Object

DFX treatment also caused a significant reduction in infiltrating CD163-positive and HO-1 positive cell in the hematoma at day 3 (Figs. 6A and B) and day 7 (Suppl Figures II & III). PubMed:27125525

Appears in Networks:
Annotations
MeSH
Cerebral Hemorrhage
Text Location
Results

p(HGNC:HMOX1) negativeCorrelation a(CHEBI:"desferrioxamine B") View Subject | View Object

Western blot analysis showed that the protein expression of HO-1 was decreased in the hematoma in the DFX treated group at day 3( HO-1/GAPDH: 0.32 ± 0.04 vs. 0.98 ± 0.07 in the vehicle-treated group, p<0.05, Fig. 6B) and day 7 (p<0.05, Suppl Figure III). PubMed:27125525

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MeSH
Cerebral Hemorrhage
Text Location
Results

p(HGNC:HMOX1) positiveCorrelation a(HM:erythrophagocytosis) View Subject | View Object

A recent study, however, indicated that HO-1 is associated with blood clearance by enhancing erythrophagocytosis after stroke. PubMed:27125525

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Cell Ontology (CL)
macrophage
MeSH
Stroke
Text Location
Discussion

p(HGNC:HMOX1) positiveCorrelation complex(a(CHEBI:heme), p(HGNC:ALB)) View Subject | View Object

In endothelial cells, we found that, in the absence of serum, heme-albumin triggered a dose-dependent HMOX1 protein expression signal in an exposure range of 0–175 lmolL1. PubMed:29610666

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Cell Ontology (CL)
endothelial cell
MeSH
Mitochondria
Text Location
Results

p(HGNC:HMOX1) positiveCorrelation complex(a(CHEBI:heme), p(HGNC:ALB)) View Subject | View Object

heme-albumin is also a robust inducer of dose-dependent HMOX1 expression in BMDMs (Figure 2D). PubMed:29610666

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Cell Ontology (CL)
endothelial cell
MeSH
Mitochondria
Text Location
Results

p(HGNC:HMOX1) positiveCorrelation complex(a(CHEBI:heme), p(HGNC:ALB)) View Subject | View Object

heme-albumin, in contrast, induced HMOX1 in a dose-dependent manner. PubMed:29610666

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Mitochondria
Text Location
Results

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.