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a(HBP:Excitotoxicity)

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Entity

Name
Excitotoxicity
Namespace
HBP
Namespace Version
20181023
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/3074b85b858455d8eeb76cfcdef685ced19bbe11/export/hbp-names.belns

Appears in Networks 3

Alzheimer's Disease: Targeting the Cholinergic System v1.0.0

Tau clearance mechanisms and their possible role in the pathogenesis of Alzheimer disease v1.0.0

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

In-Edges 4

a(CHEBI:memantine) decreases a(HBP:Excitotoxicity) View Subject | View Object

In fact, memantine is able to reduce the excitotoxicity in AD PubMed:26813123

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(p(HGNCGENEFAMILY:Calpains)) association a(HBP:Excitotoxicity) View Subject | View Object

Increasing intracellular calcium levels in PC12 cells leads to calpain-induced cleavage of tau (18). This may reflect a potential effect of excitotoxicity in AD. Inducing apoptosis in cerebellar granule cells yields calpain-mediated tau fragments, including a dominant ∼17 kDa fragment (17). PubMed:24027553

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
PC12
Text Location
Review

p(HGNC:DAPK1) positiveCorrelation a(HBP:Excitotoxicity) View Subject | View Object

In contrast, Pin1/PINN-1 (a DAPK interaction-partner and a peptidyl-prolyl isomerase involved in chronic neurodegenerative conditions) suppresses neurodegeneration in our excitotoxicity model. PubMed:25899010

Appears in Networks:

p(HGNC:PIN1) decreases a(HBP:Excitotoxicity) View Subject | View Object

In contrast, Pin1/PINN-1 (a DAPK interaction-partner and a peptidyl-prolyl isomerase involved in chronic neurodegenerative conditions) suppresses neurodegeneration in our excitotoxicity model. PubMed:25899010

Appears in Networks:

Out-Edges 2

a(HBP:Excitotoxicity) association act(p(HGNCGENEFAMILY:Calpains)) View Subject | View Object

Increasing intracellular calcium levels in PC12 cells leads to calpain-induced cleavage of tau (18). This may reflect a potential effect of excitotoxicity in AD. Inducing apoptosis in cerebellar granule cells yields calpain-mediated tau fragments, including a dominant ∼17 kDa fragment (17). PubMed:24027553

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
PC12
Text Location
Review

a(HBP:Excitotoxicity) positiveCorrelation p(HGNC:DAPK1) View Subject | View Object

In contrast, Pin1/PINN-1 (a DAPK interaction-partner and a peptidyl-prolyl isomerase involved in chronic neurodegenerative conditions) suppresses neurodegeneration in our excitotoxicity model. PubMed:25899010

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.