1. Catalog
  2. Nodes
  3. p(MGI:Hmox1)

p(MGI:Hmox1)

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
Hmox1
Namespace
mgi
Namespace Version
20181021
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/f2f993e599694ab5ce989cc39d789a499f75db99/external/mgi-names.belns

Appears in Networks 2

Adenosine A1 receptor antagonist 64627 alleviates axonopathy caused by human Tau ΔK280 v1.0.0

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 33

p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) negativeCorrelation p(MGI:Hmox1) View Subject | View Object

Surprisingly, expression of neuronal activity marker cFos, astrocytic activity marker Gfap, and oxidative stress marker Hmox1 were reduced in the proaggregant Tau transgenic slices, whereas antiaggregant Tau transgenic slices were not different from littermate controls (Fig. 4A) PubMed:27671637

Appears in Networks:

a(CHEBI:heme) negativeCorrelation p(MGI:Hmox1) View Subject | View Object

The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis. PubMed:24464629

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

a(CHEBI:heme) increases p(MGI:Hmox1) View Subject | View Object

Heme induced the expression of Ho1 and Blvrb as well as Slc40a1, which encodes the mammalian iron exporter (Figure 5A), in agreement with previous reports (Delaby et al., 2008). PubMed:24630724

Appears in Networks:
Annotations
Text Location
Results

a(CHEBI:heme) negativeCorrelation p(MGI:Hmox1) View Subject | View Object

The Hmox1 (− /− ) MEF cells expressed no functional Hmox1 mRNA (Figure 1a) and as a result accumulated more cell-associated heme during extracellular exposure compared with wild-type cells (Figure 1b). PubMed:25301065

Appears in Networks:
Annotations
Text Location
Results

a(CHEBI:heme) increases p(MGI:Hmox1) View Subject | View Object

Exposure to Hb and its oxidized products increases heme overload on the AT1 cells. Heme overload induces the expression of HO-1 and iron-sequestering proteins, such as ferritin. PubMed:26974230

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

a(CHEBI:methemoglobin) increases p(MGI:Hmox1) View Subject | View Object

Exposure to ferric Hb (HbFe31) induced a significant expression in HO-1 protein– (15.1761.04-fold) when compared with HbFe21 (9.3260.76-fold)- induced expression (Figure 2C). PubMed:26974230

Appears in Networks:
Annotations
MeSH
Alveolar Epithelial Cells
Text Location
Results

a(CHEBI:methemoglobin) increases p(MGI:Hmox1) View Subject | View Object

We found a significant enrichment of HO-1 in the mitochondrial, but not in the cytosolic fractions after exposure to HbFe21 and HbFe31 (Figures 3A and 3B). PubMed:26974230

Appears in Networks:
Annotations
MeSH
Mitochondria
Text Location
Results

a(CHEBI:protoporphyrin) increases p(MGI:Hmox1) View Subject | View Object

In contrast, PPIX treatment of macrophages was capable of inducing Hmox-1 expression (Fig. 7C), indicating that PPIX was taken up by macrophages and catabolized (13). PubMed:29212341

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

a(MESH:"Lipid Peroxides") negativeCorrelation p(MGI:Hmox1) View Subject | View Object

Accordingly, higher levels of lipid peroxide-protein adducts were detected in heme-treated Hmox1 (− /−) than in Hmox1 (+/+) MEF cells when the cells were heme exposed in the presence of an alkyne-tagged analog of linoleic acid, which is an unsaturated, heme-reactive fatty acid (Supplementary Figure 3). PubMed:25301065

Appears in Networks:
Annotations
Text Location
Results

a(MESH:ferrylhemoglobin) increases p(MGI:Hmox1) View Subject | View Object

Exposure to HbFe41 caused a significant up-regulation of HO-1 within 12 hours when compared with HbFe21 and HbFe31 (Figures 4A and 4B). PubMed:26974230

Appears in Networks:
Annotations
MeSH
Mitochondria
Text Location
Results

a(MESH:ferrylhemoglobin) increases p(MGI:Hmox1) View Subject | View Object

We found significant enrichment of HO-1 in mitochondrial fraction after exposure to HbFe31 and HbFe41 (Figure 4C). PubMed:26974230

Appears in Networks:
Annotations
MeSH
Mitochondria
Text Location
Results

p(HGNC:HBB) increases p(MGI:Hmox1) View Subject | View Object

We found a significant enrichment of HO-1 in the mitochondrial, but not in the cytosolic fractions after exposure to HbFe21 and HbFe31 (Figures 3A and 3B). PubMed:26974230

Appears in Networks:
Annotations
MeSH
Mitochondria
Text Location
Results

complex(a(CHEBI:acetylcysteine), a(CHEBI:heme)) decreases p(MGI:Hmox1) View Subject | View Object

In parallel to ferroportin, the expression of Hmox-1 was increased by heme-triggered ROS production and its induction was prevented by the combined treatment with NAC and heme (Fig. 8B). PubMed:29212341

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

complex(a(CHEBI:acetylcysteine), a(CHEBI:heme)) decreases p(MGI:Hmox1) View Subject | View Object

Similarly, the induction of Hmox1 by heme was abolished by cotreatment with NAC and heme, supporting our in vitro findings (Fig. 8D). PubMed:29212341

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

p(MGI:Hpx) decreases p(MGI:Hmox1) View Subject | View Object

We found that Hpx effectively attenuated HO-1 induction by all redox forms of Hb. PubMed:26974230

Appears in Networks:
Annotations
MeSH
Mitochondria
Text Location
Results

p(MGI:Hpx) decreases p(MGI:Hmox1) View Subject | View Object

Consistently, HO-1 mRNA and protein levels were higher in hearts from Hx-/- mice than in controls (Figure 2B). Immunohistochemistry for HO-1 on heart sections indicated higher HO-1 expression in cardiomyocytes from Hx-/- mice than in wild-type animals (Figure 2B). PubMed:28400318

Appears in Networks:
Annotations
Cell Ontology (CL)
regular cardiac myocyte
Text Location
Results

complex(a(MESH:"Blood Transfusion"), p(MGI:Alb)) positiveCorrelation p(MGI:Hmox1) View Subject | View Object

Mice that were resuscitated with SRBCs and albumin or SRBCs and hemopexin showed a marked increase in HO-1 expression when compared to mice resuscitated with FRBCs. PubMed:27515135

Appears in Networks:
Annotations
MeSH
Kidney
MeSH
Hemorrhage
Text Location
Results

p(MGI:Alb) causesNoChange p(MGI:Hmox1) View Subject | View Object

In contrast, albumin did not induce HO-1 or inhibit stasis and NF- κB. PubMed:29694434

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

complex(a(MESH:"Blood Transfusion"), p(MGI:Hp)) negativeCorrelation p(MGI:Hmox1) View Subject | View Object

Resuscitation with SRBCs and haptoglobin prevented the increase in SRBC-induced renal HO-1 expression (Figure 7F). PubMed:27515135

Appears in Networks:
Annotations
MeSH
Kidney
MeSH
Hemorrhage
Text Location
Results

p(MGI:Hp) decreases p(MGI:Hmox1) View Subject | View Object

Hp attenuated HbFe21- and HbFe31-induced up-regulation of HO-1 and H-ferritin proteins (Figure 2B). PubMed:26974230

Appears in Networks:
Annotations
MeSH
Alveolar Epithelial Cells
Text Location
Results

p(MGI:Hp) decreases p(MGI:Hmox1) View Subject | View Object

Interestingly, Hp attenuated the HbFe21- and HbFe31-induced HO-1 expression in the mitochondria (Figures 3A and 3B). PubMed:26974230

Appears in Networks:
Annotations
MeSH
Mitochondria
Text Location
Results

complex(a(MESH:"Blood Transfusion"), p(MGI:Hpx)) positiveCorrelation p(MGI:Hmox1) View Subject | View Object

Mice that were resuscitated with SRBCs and albumin or SRBCs and hemopexin showed a marked increase in HO-1 expression when compared to mice resuscitated with FRBCs. PubMed:27515135

Appears in Networks:
Annotations
MeSH
Kidney
MeSH
Hemorrhage
Text Location
Results

p(MGI:Casp1) negativeCorrelation p(MGI:Hmox1) View Subject | View Object

The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis. PubMed:24464629

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

p(MGI:Cox4i1) negativeCorrelation p(MGI:Hmox1) View Subject | View Object

However, hemin or LPS-induced mitochondrial accumulation of HO-1 was associated with decreased mitochondrial heme content and reduced expression of heme-sensitive subunit I of complex IV with loss of activity (33). PubMed:26974230

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

p(MGI:Il1b) negativeCorrelation p(MGI:Hmox1) View Subject | View Object

The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis. PubMed:24464629

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

p(MGI:Nlrp3) negativeCorrelation p(MGI:Hmox1) View Subject | View Object

The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis. PubMed:24464629

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

path(HM:"vaso-occlusive crisis") negativeCorrelation p(MGI:Hmox1) View Subject | View Object

We have previously shown that induction of HO-1 expression or liver-directed HO-1 gene therapy inhibits stasis in sickle mice exposed to H/R [38, 45]. PubMed:29694434

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

path(MESH:"Acute Kidney Injury") negativeCorrelation p(MGI:Hmox1) View Subject | View Object

For instance, Hmox−/− mice develops acute renal failure and marked mortality when submitted to rhabdomyolysis, a pathological condition that increases serum myoglobin which can be oxidized and release heme (Nath et al., 2000). PubMed:24904418

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

path(MESH:"Insulin Resistance") negativeCorrelation p(MGI:Hmox1) View Subject | View Object

Furthermore, Hmox1−/− mice are susceptible to liver IR which is characterized by tissue damage in sites that are reperfused after ischemia injury and hemolysis (Devey et al., 2009). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Rhabdomyolysis
Text Location
Review

path(MESH:"Mitochondrial Diseases") negativeCorrelation p(MGI:Hmox1) View Subject | View Object

During heme exposure the Hmox1 (−/ −) cells show a dose-dependent decrease in mitochondrial function as indicated by decreased cellular ATP (Figure 1c) and parallel induction of caspase 3/7 activity (Figure 1d) as well as nuclear condensation (Figure 1e) that occurred at heme concentrations exceeding 10 μM. PubMed:25301065

Appears in Networks:
Annotations
Text Location
Results

path(MESH:"Porphyria, Erythropoietic") positiveCorrelation p(MGI:Hmox1) View Subject | View Object

Moreover, HO-1 was highly expressed in the liver of CEP compared to WT mice (Figure 4E), confirming that residual heme uptake is rapidly degraded in the liver. PubMed:28143953

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Porphyria, Erythropoietic
Text Location
Results

path(MESH:"Vascular System Injuries") negativeCorrelation p(MGI:Hmox1) View Subject | View Object

Clinical studies have confirmed endothelial dysfunction and vasculopathy in a patient with HO-1 deficiency, and similarly, mice lacking HO-1 have increased vascular injury and thrombotic complications (43, 44). PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
Text Location
Discussion

path(MESH:Thrombosis) negativeCorrelation p(MGI:Hmox1) View Subject | View Object

Clinical studies have confirmed endothelial dysfunction and vasculopathy in a patient with HO-1 deficiency, and similarly, mice lacking HO-1 have increased vascular injury and thrombotic complications (43, 44). PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
Text Location
Discussion

Out-Edges 27

p(MGI:Hmox1) negativeCorrelation p(HBP:"Tau isoform F (441 aa)", var("p.Lys280del")) View Subject | View Object

Surprisingly, expression of neuronal activity marker cFos, astrocytic activity marker Gfap, and oxidative stress marker Hmox1 were reduced in the proaggregant Tau transgenic slices, whereas antiaggregant Tau transgenic slices were not different from littermate controls (Fig. 4A) PubMed:27671637

Appears in Networks:

p(MGI:Hmox1) biomarkerFor bp(GO:"response to oxidative stress") View Subject | View Object

Surprisingly, expression of neuronal activity marker cFos, astrocytic activity marker Gfap, and oxidative stress marker Hmox1 were reduced in the proaggregant Tau transgenic slices, whereas antiaggregant Tau transgenic slices were not different from littermate controls (Fig. 4A) PubMed:27671637

Appears in Networks:

p(MGI:Hmox1) decreases a(CHEBI:heme) View Subject | View Object

Mice lacking HO-1 (Hmox1−/−) are highly susceptible to pathologic conditions associated with increased serum heme concentration. PubMed:24904418

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

p(MGI:Hmox1) negativeCorrelation path(MESH:"Vascular System Injuries") View Subject | View Object

Clinical studies have confirmed endothelial dysfunction and vasculopathy in a patient with HO-1 deficiency, and similarly, mice lacking HO-1 have increased vascular injury and thrombotic complications (43, 44). PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
Text Location
Discussion

p(MGI:Hmox1) negativeCorrelation path(MESH:Thrombosis) View Subject | View Object

Clinical studies have confirmed endothelial dysfunction and vasculopathy in a patient with HO-1 deficiency, and similarly, mice lacking HO-1 have increased vascular injury and thrombotic complications (43, 44). PubMed:19276082

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Aorta
Text Location
Discussion

p(MGI:Hmox1) negativeCorrelation a(CHEBI:heme) View Subject | View Object

The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis. PubMed:24464629

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

p(MGI:Hmox1) negativeCorrelation a(CHEBI:heme) View Subject | View Object

The Hmox1 (− /− ) MEF cells expressed no functional Hmox1 mRNA (Figure 1a) and as a result accumulated more cell-associated heme during extracellular exposure compared with wild-type cells (Figure 1b). PubMed:25301065

Appears in Networks:
Annotations
Text Location
Results

p(MGI:Hmox1) increases deg(a(CHEBI:heme)) View Subject | View Object

Macrophages are crucial for the removal of excess heme resulting from hemolysis via the uptake and degradation of heme by HO-1 (ref. 23), encoded by Hmox1. PubMed:27798618

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

p(MGI:Hmox1) decreases path(MESH:Inflammation) View Subject | View Object

The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis. PubMed:24464629

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

p(MGI:Hmox1) negativeCorrelation p(MGI:Nlrp3) View Subject | View Object

The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis. PubMed:24464629

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

p(MGI:Hmox1) negativeCorrelation p(MGI:Casp1) View Subject | View Object

The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis. PubMed:24464629

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

p(MGI:Hmox1) negativeCorrelation p(MGI:Il1b) View Subject | View Object

The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis. PubMed:24464629

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

p(MGI:Hmox1) negativeCorrelation path(MESH:"Acute Kidney Injury") View Subject | View Object

For instance, Hmox−/− mice develops acute renal failure and marked mortality when submitted to rhabdomyolysis, a pathological condition that increases serum myoglobin which can be oxidized and release heme (Nath et al., 2000). PubMed:24904418

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

p(MGI:Hmox1) negativeCorrelation path(MESH:"Insulin Resistance") View Subject | View Object

Furthermore, Hmox1−/− mice are susceptible to liver IR which is characterized by tissue damage in sites that are reperfused after ischemia injury and hemolysis (Devey et al., 2009). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Rhabdomyolysis
Text Location
Review

p(MGI:Hmox1) negativeCorrelation path(MESH:"Mitochondrial Diseases") View Subject | View Object

During heme exposure the Hmox1 (−/ −) cells show a dose-dependent decrease in mitochondrial function as indicated by decreased cellular ATP (Figure 1c) and parallel induction of caspase 3/7 activity (Figure 1d) as well as nuclear condensation (Figure 1e) that occurred at heme concentrations exceeding 10 μM. PubMed:25301065

Appears in Networks:
Annotations
Text Location
Results

p(MGI:Hmox1) decreases p(MGI:Sqstm1) View Subject | View Object

We confirmed by selected reaction monitoring (SRM) mode mass spectrometry (Figure 3a) and western blot (Figures 3c and d), respectively, that heme increased Sqstm1, ubiquitin, and Hsp70, with a much stronger response in Hmox1 (−/− ) compared with Hmox1 (+/+) MEF cells. PubMed:25301065

Appears in Networks:
Annotations
Text Location
Results

p(MGI:Hmox1) decreases p(PFAM:ubiquitin) View Subject | View Object

We confirmed by selected reaction monitoring (SRM) mode mass spectrometry (Figure 3a) and western blot (Figures 3c and d), respectively, that heme increased Sqstm1, ubiquitin, and Hsp70, with a much stronger response in Hmox1 (−/− ) compared with Hmox1 (+/+) MEF cells. PubMed:25301065

Appears in Networks:
Annotations
Text Location
Results

p(MGI:Hmox1) decreases p(MGI:Hspa2) View Subject | View Object

We confirmed by selected reaction monitoring (SRM) mode mass spectrometry (Figure 3a) and western blot (Figures 3c and d), respectively, that heme increased Sqstm1, ubiquitin, and Hsp70, with a much stronger response in Hmox1 (−/− ) compared with Hmox1 (+/+) MEF cells. PubMed:25301065

Appears in Networks:
Annotations
Text Location
Results

p(MGI:Hmox1) negativeCorrelation a(MESH:"Lipid Peroxides") View Subject | View Object

Accordingly, higher levels of lipid peroxide-protein adducts were detected in heme-treated Hmox1 (− /−) than in Hmox1 (+/+) MEF cells when the cells were heme exposed in the presence of an alkyne-tagged analog of linoleic acid, which is an unsaturated, heme-reactive fatty acid (Supplementary Figure 3). PubMed:25301065

Appears in Networks:
Annotations
Text Location
Results

p(MGI:Hmox1) decreases bp(MESH:"Oxidative Stress") View Subject | View Object

A recent study indicated that expression of HO-1 targeted to mitochondria attenuated oxidative stress (43). PubMed:26974230

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

p(MGI:Hmox1) negativeCorrelation p(MGI:Cox4i1) View Subject | View Object

However, hemin or LPS-induced mitochondrial accumulation of HO-1 was associated with decreased mitochondrial heme content and reduced expression of heme-sensitive subunit I of complex IV with loss of activity (33). PubMed:26974230

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

p(MGI:Hmox1) increases a(CHEBI:"carbon monoxide") View Subject | View Object

Moreover, mitochondrial translocation of HO-1 can also lead to localized CO production as a result of heme degradation, thus inhibiting electron flow though mitochondrial electron transport chain complex IV (44). PubMed:26974230

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

p(MGI:Hmox1) positiveCorrelation complex(a(MESH:"Blood Transfusion"), p(MGI:Hpx)) View Subject | View Object

Mice that were resuscitated with SRBCs and albumin or SRBCs and hemopexin showed a marked increase in HO-1 expression when compared to mice resuscitated with FRBCs. PubMed:27515135

Appears in Networks:
Annotations
MeSH
Kidney
MeSH
Hemorrhage
Text Location
Results

p(MGI:Hmox1) positiveCorrelation complex(a(MESH:"Blood Transfusion"), p(MGI:Alb)) View Subject | View Object

Mice that were resuscitated with SRBCs and albumin or SRBCs and hemopexin showed a marked increase in HO-1 expression when compared to mice resuscitated with FRBCs. PubMed:27515135

Appears in Networks:
Annotations
MeSH
Kidney
MeSH
Hemorrhage
Text Location
Results

p(MGI:Hmox1) negativeCorrelation complex(a(MESH:"Blood Transfusion"), p(MGI:Hp)) View Subject | View Object

Resuscitation with SRBCs and haptoglobin prevented the increase in SRBC-induced renal HO-1 expression (Figure 7F). PubMed:27515135

Appears in Networks:
Annotations
MeSH
Kidney
MeSH
Hemorrhage
Text Location
Results

p(MGI:Hmox1) positiveCorrelation path(MESH:"Porphyria, Erythropoietic") View Subject | View Object

Moreover, HO-1 was highly expressed in the liver of CEP compared to WT mice (Figure 4E), confirming that residual heme uptake is rapidly degraded in the liver. PubMed:28143953

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Porphyria, Erythropoietic
Text Location
Results

p(MGI:Hmox1) negativeCorrelation path(HM:"vaso-occlusive crisis") View Subject | View Object

We have previously shown that induction of HO-1 expression or liver-directed HO-1 gene therapy inhibits stasis in sickle mice exposed to H/R [38, 45]. PubMed:29694434

Appears in Networks:
Annotations
MeSH
Liver
MeSH
Anemia, Sickle Cell
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.