1. Catalog
  2. Nodes
  3. p(HBP:"APOE e4")

p(HBP:"APOE e4")

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

Entity

Name
APOE e4
Namespace
HBP
Namespace Version
20181029
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/785431732a26d6809b4162d98b95687d16404e63/export/hbp-names.belns

Appears in Networks 3

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

Clearance systems in the brain-implications for Alzheimer disease. v1.0.1

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 3

a(CHEBI:estrogen) decreases act(p(HBP:"APOE e4")) View Subject | View Object

ApoE-epsilon4, but not ApoE-epsilon3, disrupts carbachol-stimulated phosphoinositol (PI) hydrolysis and so does Abeta and Abeta/ApoE-epsilon4 complexes in SH-SY5Y cells (Cedazo- Mínguez and Cowburn, 2001). The effect of Abeta and its ApoE complex on PI hydrolysis were blocked by estrogen, and this disruption was itself blocked by wortmannin, suggesting that PI3K mediates estrogen’s effect on PI hydrolysis. PubMed:19293145

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

path(MESH:"Alzheimer Disease") association p(HBP:"APOE e4") View Subject | View Object

The strongest identified genetic risk factor for LOAD is the apolipoprotein E (APOE) ε4 allele (APOE*ε4), PubMed:26195256

Appears in Networks:

complex(GO:"protein phosphatase type 2A complex") negativeCorrelation p(HBP:"APOE e4") View Subject | View Object

Our results indicated a significant down-regulation of PPP2R5E gene expression and reduction in PP2A activity by ApoE4 compared with ApoE3. This may also explain an elevated Tau phosphorylation in AD human brains that featured at least one ApoE4 allele. PubMed:28720530

Appears in Networks:

Out-Edges 12

p(HBP:"APOE e4") decreases act(a(CHEBI:carbachol), ma(MESH:Hydrolysis)) View Subject | View Object

ApoE-epsilon4, but not ApoE-epsilon3, disrupts carbachol-stimulated phosphoinositol (PI) hydrolysis and so does Abeta and Abeta/ApoE-epsilon4 complexes in SH-SY5Y cells (Cedazo- Mínguez and Cowburn, 2001). The effect of Abeta and its ApoE complex on PI hydrolysis were blocked by estrogen, and this disruption was itself blocked by wortmannin, suggesting that PI3K mediates estrogen’s effect on PI hydrolysis. PubMed:19293145

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

p(HBP:"APOE e4") association path(MESH:"Alzheimer Disease") View Subject | View Object

The strongest identified genetic risk factor for LOAD is the apolipoprotein E (APOE) ε4 allele (APOE*ε4), PubMed:26195256

Appears in Networks:

p(HBP:"APOE e4") regulates a(MESH:"Blood-Brain Barrier") View Subject | View Object

Third, ApoE4 is also associated with lower antioxidant activity than other ApoE isoforms,154,155 and it mediates BBB breakdown through a proinflammatory pathway involving cyclophilin A in pericytes. PubMed:26195256

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Temporal Lobe

p(HBP:"APOE e4") decreases bp(HBP:"perivascular drainage pathways") View Subject | View Object

The pres- ence of ApoE4 is associated with reduced perivascular drainage of Aβ,161 which in turn is linked to deposition of immune complexes. PubMed:26195256

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Temporal Lobe

p(HBP:"APOE e4") increases p(MGI:Capn2) View Subject | View Object

The levels of CDK5, its regulatory subunits (p35 and p25) and calpain (including calpain1 and calpain2), but not GSK3ß, were significantly increased in E4FAD mice compared to E3FAD mice. PubMed:27087442

Appears in Networks:

p(HBP:"APOE e4") increases p(MGI:Cdk5) View Subject | View Object

The levels of CDK5, its regulatory subunits (p35 and p25) and calpain (including calpain1 and calpain2), but not GSK3ß, were significantly increased in E4FAD mice compared to E3FAD mice. PubMed:27087442

Appears in Networks:

p(HBP:"APOE e4") increases p(HBP:"CDK5R1 p25") View Subject | View Object

The levels of CDK5, its regulatory subunits (p35 and p25) and calpain (including calpain1 and calpain2), but not GSK3ß, were significantly increased in E4FAD mice compared to E3FAD mice. PubMed:27087442

Appears in Networks:

p(HBP:"APOE e4") increases p(MGI:Cdk5r1) View Subject | View Object

The levels of CDK5, its regulatory subunits (p35 and p25) and calpain (including calpain1 and calpain2), but not GSK3ß, were significantly increased in E4FAD mice compared to E3FAD mice. PubMed:27087442

Appears in Networks:

p(HBP:"APOE e4") increases p(MGI:Capn1) View Subject | View Object

The levels of CDK5, its regulatory subunits (p35 and p25) and calpain (including calpain1 and calpain2), but not GSK3ß, were significantly increased in E4FAD mice compared to E3FAD mice. PubMed:27087442

Appears in Networks:

p(HBP:"APOE e4") causesNoChange p(MGI:Gsk3b) View Subject | View Object

The levels of CDK5, its regulatory subunits (p35 and p25) and calpain (including calpain1 and calpain2), but not GSK3ß, were significantly increased in E4FAD mice compared to E3FAD mice. PubMed:27087442

Appears in Networks:

p(HBP:"APOE e4") directlyDecreases p(HGNC:PPP2R5E) View Subject | View Object

Our results indicated a significant down-regulation of PPP2R5E gene expression and reduction in PP2A activity by ApoE4 compared with ApoE3. This may also explain an elevated Tau phosphorylation in AD human brains that featured at least one ApoE4 allele. PubMed:28720530

Appears in Networks:

p(HBP:"APOE e4") negativeCorrelation complex(GO:"protein phosphatase type 2A complex") View Subject | View Object

Our results indicated a significant down-regulation of PPP2R5E gene expression and reduction in PP2A activity by ApoE4 compared with ApoE3. This may also explain an elevated Tau phosphorylation in AD human brains that featured at least one ApoE4 allele. PubMed:28720530

Appears in Networks:

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.