1. Catalog
  2. Nodes
  3. a(CHEBI:cholesterol)

a(CHEBI:cholesterol)

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

Entity

Name
cholesterol
Namespace
chebi
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/chebi-names.belns

Appears in Networks 5

Nuclear receptors as therapeutic targets for Alzheimer's disease. v1.0.0

Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system v1.0.0

This document contains the curation of the review article Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system by Taly et al. 2009

Alzheimer’s disease and the autophagic-lysosomal system v1.0.0

The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 4

act(p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) association a(CHEBI:cholesterol) View Subject | View Object

Cholesterol is known to be crucial to nAChR function, and it interacts within the transmembrane domain between TM1, TM3 and TM4 (ReF. 57). PubMed:19721446

Appears in Networks:
Annotations
Text Location
Review

bp(GO:endocytosis) positiveCorrelation a(CHEBI:cholesterol) View Subject | View Object

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

Appears in Networks:

p(HBP:"APP C-terminally truncated carboxyl-terminal fragments") positiveCorrelation a(CHEBI:cholesterol) View Subject | View Object

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

Appears in Networks:

a(HM:"Atheroma lipid") positiveCorrelation a(CHEBI:cholesterol) View Subject | View Object

Elevated cholesterol, oxy-cholesterol, lyso-phospholipid and decreased phosphatidylserine were found in atheromatous lipids compared to controls (supplemental Table II). PubMed:20378845

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

Out-Edges 8

a(CHEBI:cholesterol) increases act(p(HGNC:NR1H3)) View Subject | View Object

LXR receptors are activated by oxysterols, most prominently hydroxylated forms of cholesterol, and play a critical role in the control of whole body cholesterol homeostasis, as well as exerting potent anti-inflammatory actions [26]. PubMed:21718217

Appears in Networks:
Annotations
Confidence
Medium

a(CHEBI:cholesterol) association act(p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits")) View Subject | View Object

Cholesterol is known to be crucial to nAChR function, and it interacts within the transmembrane domain between TM1, TM3 and TM4 (ReF. 57). PubMed:19721446

Appears in Networks:
Annotations
Text Location
Review

a(CHEBI:cholesterol) increases a(MESH:"Amyloid beta-Peptides") View Subject | View Object

Cellular cholesterol can directly impact the level of Aβ, as decreases in cholesterol levels inhibit the generation of Aβ peptides through direct modulation of γ-secretase activity [78,79]. PubMed:29758300

Appears in Networks:

a(CHEBI:cholesterol) regulates act(complex(GO:"gamma-secretase complex")) View Subject | View Object

Cellular cholesterol can directly impact the level of Aβ, as decreases in cholesterol levels inhibit the generation of Aβ peptides through direct modulation of γ-secretase activity [78,79]. PubMed:29758300

Appears in Networks:

a(CHEBI:cholesterol) positiveCorrelation p(HBP:"APP C-terminally truncated carboxyl-terminal fragments") View Subject | View Object

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

Appears in Networks:

a(CHEBI:cholesterol) positiveCorrelation bp(GO:endocytosis) View Subject | View Object

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

Appears in Networks:

a(CHEBI:cholesterol) increases a(GO:endosome) View Subject | View Object

In this regard, elevated bCTF levels induced by APP overexpression, elevated dietary cholesterol, or overexpression of its receptor ApoE (particularly ApoE 14) can upregulate endocytosis and enlarge endosomes (Laifenfeld et al. 2007; Chen et al. 2010; Cossec et al. 2010), leading to impaired endosome retrograde transport (S Kim and RA Nixon, unpubl.). PubMed:22908190

Appears in Networks:

a(CHEBI:cholesterol) positiveCorrelation a(HM:"Atheroma lipid") View Subject | View Object

Elevated cholesterol, oxy-cholesterol, lyso-phospholipid and decreased phosphatidylserine were found in atheromatous lipids compared to controls (supplemental Table II). PubMed:20378845

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