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bp(GO:"complement activation, alternative pathway")

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Entity

Name
complement activation, alternative pathway
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 1

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 6

a(CHEBI:heme) increases bp(GO:"complement activation, alternative pathway") View Subject | View Object

It is possible that heme-induced overactivation of the alternative complement pathway, and depo- sition of C3 fragments on erythrocyte membranes, participate in erythrophagocytosis of uninfected red blood cells in severe forms of malaria [77]. PubMed:26875449

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

a(CHEBI:heme) increases bp(GO:"complement activation, alternative pathway") View Subject | View Object

Heme exposure of other proteins in the alternative pathway (factors B, D, and H) does not appear to have any impact on their functions, thus implying that heme activates the alternative complement pathway by affecting C3 directly [33]. PubMed:26875449

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

a(CHEBI:heme) increases bp(GO:"complement activation, alternative pathway") View Subject | View Object

The inhibitory effect of heme on the classical pathway is in agreement with in vitro functional assays showing that heme is capable of activating only the alternative pathway in human sera. PubMed:26875449

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

a(CHEBI:heme) increases bp(GO:"complement activation, alternative pathway") View Subject | View Object

In contrast to its overactivating effects on the alternative pathway, heme inhibits the classical pathway. It binds to C1q, alters its electrostatic properties, and hampers the recognition of target molecules. This results in a reduction of classical pathway C3 convertase formation and C3b deposition. PubMed:26875449

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

a(HM:erythrophagocytosis) positiveCorrelation bp(GO:"complement activation, alternative pathway") View Subject | View Object

It is possible that heme-induced overactivation of the alternative complement pathway, and depo- sition of C3 fragments on erythrocyte membranes, participate in erythrophagocytosis of uninfected red blood cells in severe forms of malaria [77]. PubMed:26875449

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

path(MESH:"Atypical Hemolytic Uremic Syndrome") positiveCorrelation bp(GO:"complement activation, alternative pathway") View Subject | View Object

Atypical hemolytic uremic syndrome (aHUS) is characterized by an over activation of the complement alternative pathway (CAP) due to genetic and acquired abnormalities (Noris and Remuzzi, 2009). PubMed:24904418

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

Out-Edges 2

bp(GO:"complement activation, alternative pathway") positiveCorrelation path(MESH:"Atypical Hemolytic Uremic Syndrome") View Subject | View Object

Atypical hemolytic uremic syndrome (aHUS) is characterized by an over activation of the complement alternative pathway (CAP) due to genetic and acquired abnormalities (Noris and Remuzzi, 2009). PubMed:24904418

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

bp(GO:"complement activation, alternative pathway") positiveCorrelation a(HM:erythrophagocytosis) View Subject | View Object

It is possible that heme-induced overactivation of the alternative complement pathway, and depo- sition of C3 fragments on erythrocyte membranes, participate in erythrophagocytosis of uninfected red blood cells in severe forms of malaria [77]. PubMed:26875449

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

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.