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Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 9

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

Furthermore, haem-induced release of P-selectin and VWF is mediated by TLR4 and NFkB signalling. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

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

Heme activates endothelial cells inducing the expression of the adhesion molecules ICAM-1 (intercellular adhesion molecule 1), VCAM-1 (vascular cell adhesion molecule 1), E-selectin, Pselectin, and von Willebrand factor (VWF; Wagener et al., 1997; Belcher et al., 2014) and causes neutrophil migration (GraçaSouza et al., 2002; Porto et al., 2007). PubMed:24904418

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

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

In endothelial cells, heme induces TLR4-dependent degranulation of Weibel–Palade bodies and P-selectins and VWF release. PubMed:24904418

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

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

For example, haem stimulates expression of P-selectin and von Willebrand Factor (VWF) ‘strings’ on endothelial cells in vitro and on the vessel walls of both normal and SCD mice (Belcher et al, 2014). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

bp(HM:"Monocyte–platelet aggregation") positiveCorrelation p(HGNC:SELP) View Subject | View Object

Monocyte–platelet interactions are believed to be predominantly mediated by surface P-selectin/integrins and their receptors, and it was suggested that monocyte-platelet aggregates are a marker of platelet activation as well as a pathway for the regulation of monocyte and platelet function [17]. PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Cell Ontology (CL)
neutrophil
Cell Ontology (CL)
platelet
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Results

bp(MESH:"Platelet Activation") positiveCorrelation p(HGNC:SELP) View Subject | View Object

In contrast to platelet lysis, platelet activation is clearly seen, based on both the higher expression of CD62P (Fig. 3B) and increased coaggregation with white blood cells. PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Endothelium
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Discussion

bp(MESH:"Platelet Activation") positiveCorrelation p(HGNC:SELP) View Subject | View Object

Surface accumulation of MAC may be at least partially responsible for the activated platelet phenotype seen in patients with primary Cys89Tyr CD59 mutation, as manifested both by increased CD62P expression and monocyte-platelet aggregates. PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Endothelium
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Discussion

bp(MESH:"Platelet Aggregation") positiveCorrelation p(HGNC:SELP) View Subject | View Object

In patients with SCD (Wun et al, 1998) and b-thalassaemia (Ruf et al, 1997), flow cytometry demonstrates the presence of an increased fraction of platelets expressing P-selectin, a platelet membrane receptor that mediates platelet–endothelial interactions. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

p(HGNC:CD59, var("p.Cys89Tyr")) increases p(HGNC:SELP) View Subject | View Object

Interaction between monocytes and platelets was suggested to be via p selection [17], which was shown here to be much higher in patients with primary Cys89Tyr mutation in CD59. PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Cell Ontology (CL)
neutrophil
Cell Ontology (CL)
platelet
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Results

Out-Edges 4

p(HGNC:SELP) positiveCorrelation bp(MESH:"Platelet Aggregation") View Subject | View Object

In patients with SCD (Wun et al, 1998) and b-thalassaemia (Ruf et al, 1997), flow cytometry demonstrates the presence of an increased fraction of platelets expressing P-selectin, a platelet membrane receptor that mediates platelet–endothelial interactions. PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

p(HGNC:SELP) positiveCorrelation bp(HM:"Monocyte–platelet aggregation") View Subject | View Object

Monocyte–platelet interactions are believed to be predominantly mediated by surface P-selectin/integrins and their receptors, and it was suggested that monocyte-platelet aggregates are a marker of platelet activation as well as a pathway for the regulation of monocyte and platelet function [17]. PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
Cell Ontology (CL)
neutrophil
Cell Ontology (CL)
platelet
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Results

p(HGNC:SELP) positiveCorrelation bp(MESH:"Platelet Activation") View Subject | View Object

In contrast to platelet lysis, platelet activation is clearly seen, based on both the higher expression of CD62P (Fig. 3B) and increased coaggregation with white blood cells. PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Endothelium
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Discussion

p(HGNC:SELP) positiveCorrelation bp(MESH:"Platelet Activation") View Subject | View Object

Surface accumulation of MAC may be at least partially responsible for the activated platelet phenotype seen in patients with primary Cys89Tyr CD59 mutation, as manifested both by increased CD62P expression and monocyte-platelet aggregates. PubMed:29929138

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Endothelium
MeSH
Hemoglobinuria, Paroxysmal
Text Location
Discussion

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.