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a(HBP:HBP00030)

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

Entity

Name
HBP00030
Namespace
HBP
Namespace Version
20181029
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/785431732a26d6809b4162d98b95687d16404e63/export/hbp.belns

Appears in Networks 2

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

Promoting the clearance of neurotoxic proteins in neurodegenerative disorders of ageing v1.0.0

In-Edges 1

path(MESH:"Alzheimer Disease") positiveCorrelation a(HBP:HBP00030) View Subject | View Object

The ApoE4 allele is most important genetic risk factor for AD, while the ApoE2 allele is thought to be protective. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High
MeSH
Microglia

Out-Edges 5

a(HBP:HBP00030) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

The ApoE4 allele is most important genetic risk factor for AD, while the ApoE2 allele is thought to be protective. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High
MeSH
Microglia

a(HBP:HBP00030) increases a(HBP:HBP00018) View Subject | View Object

Mice expressing the ApoE4 isoform exhibited higher levels of Ab deposition in comparison to ApoE3 or ApoE2 expressing animals [36]. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High
MeSH
Microglia

a(HBP:HBP00030) increases path(MESH:"Alzheimer Disease") View Subject | View Object

Third, apolipoprotein E allele 4 (APOE4), a major risk allele for sporadic AD, is associated with increased generation and accumula- tion of Aβ42 (REFS59,60) . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(HBP:HBP00030) increases a(CHEBI:"amyloid-beta polypeptide 42") View Subject | View Object

Third, apolipoprotein E allele 4 (APOE4), a major risk allele for sporadic AD, is associated with increased generation and accumula- tion of Aβ42 (REFS59,60) . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(HBP:HBP00030) increases p(HGNC:LGMN) View Subject | View Object

In addition to decreased degradation, one consequence is leakage of asparaginyl endopeptidase into the cytosol, where it generates toxic fragments of tau 61 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Cytosol
MeSH
Alzheimer Disease

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.