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  4. PC12

PC12

Name
PC12
Namespace Keyword
CellLine
Namespace
Experimental Factor Ontology (EFO)
Namespace Version
20170511
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/annotation/cell-line/cell-line-20170511.belanno

Sample Annotated Edges 5

a(CHEBI:nicotine) association bp(GO:"calcium-mediated signaling") View Subject | View Object

Nicotine protects PC12 cells from cell death resulting from serum depletion through a mechanism that depends upon the function of IP3 receptors, L-type calcium channels, ryanodine receptors, and ERK, suggesting that the protective effect of nicotine is mediated by calcium signaling pathways (Ren et al., 2005). PubMed:19293145

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

p(HGNC:SRC) increases bp(MESH:Neuroprotection) View Subject | View Object

Furthermore, inhibitors of SRC, a closely related tyrosine kinase, also prevent nicotinic protection of differentiated PC12 cells against serum-deprivation-induced cell death (Li et al., 1999b), and inhibitors of FYN or Janus kinase-2 (JAK-2) block the neuroprotection against Abeta toxicity of therapeutic AChE inhibitors (Takada-Takatori et al., 2006). PubMed:19293145

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

a(CHEBI:"amyloid-beta") increases p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

It is also noteworthy that Abeta-induced tau protein phosphorylation in PC12 cells is inhibited not only by alpha7 agonists, as would be predicted from the role of alpha7 nAChRs in neuroprotection, but also by alpha-bungarotoxin (Hu et al., 2008), as might be predicted if the competition by alpha-bungarotoxin for the Abeta site blocked a direct action of Abeta on nAChRs. It is therefore possible that the toxicity of Abeta is mediated, at least in part, through a direct physical interaction between Abeta and nAChRs. PubMed:19293145

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

p(HGNC:FYN) increases bp(MESH:Neuroprotection) View Subject | View Object

Furthermore, inhibitors of SRC, a closely related tyrosine kinase, also prevent nicotinic protection of differentiated PC12 cells against serum-deprivation-induced cell death (Li et al., 1999b), and inhibitors of FYN or Janus kinase-2 (JAK-2) block the neuroprotection against Abeta toxicity of therapeutic AChE inhibitors (Takada-Takatori et al., 2006). PubMed:19293145

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

act(a(CHEBI:ethanol)) increases path(HBP:neurotoxicity) View Subject | View Object

Nicotinic neuroprotection against non-Abeta toxicity is also mediated largely through alpha7 nAChRs. alpha7 nAChRs protect PC12 cells against ethanol toxicity (Li et al., 1999a) and from cell death associated with serum depletion (Ren et al., 2005); they protect cultured neurons against glutamate-induced excitotoxicity (Kaneko et al., 1997) and hippocampal slices against oxygen and glucose deprivation (Egea et al., 2007) through the activation of alpha7 nAChRs (Rosa et al., 2006). PubMed:19293145

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

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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.