Name
cerebral cortex
Namespace Keyword
Anatomy
Namespace
Uberon
Namespace Version
20170511
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/annotation/anatomy/anatomy-20170511.belanno

Sample Annotated Edges 5

a(HBP:"cerebral cortex") positiveCorrelation p(HBP:RAC1b) View Subject | View Object

Because we also found Rac1b-positive neurons in the AD cortex, it will be interesting to determine whether these perikarya display a similar gene profile to that found in the NB cholinergic neurons. PubMed:22142809

Appears in Networks:
Annotations
Uberon
cerebral cortex
Disease Ontology (DO)
Alzheimer's disease
MeSH
Alzheimer Disease

p(HBP:RAC1b) positiveCorrelation a(HBP:"cerebral cortex") View Subject | View Object

Because we also found Rac1b-positive neurons in the AD cortex, it will be interesting to determine whether these perikarya display a similar gene profile to that found in the NB cholinergic neurons. PubMed:22142809

Appears in Networks:
Annotations
Uberon
cerebral cortex
Disease Ontology (DO)
Alzheimer's disease
MeSH
Alzheimer Disease

a(CHEBI:"amyloid-beta") negativeCorrelation p(MGI:Dyrk1a) View Subject | View Object

Normalizing the gene dosage of Dyrk1A in the TS mouse rescued the density of senescent cells in the cingulate cortex, hippocampus and septum, prevented cholinergic neuron degeneration, and reduced App expression in the hippocampus, Aß load in the cortex and hippocampus, the expression of phosphorylated tau at the Ser202 residue in the hippocampus and cerebellum and the levels of total tau in the cortex, hippocampus and cerebellum. PubMed:29221819

a(CHEBI:"hydrogen peroxide") increases bp(MESH:"Oxidative Stress") View Subject | View Object

Primary cortical neurons exposed to the mitochondrial toxin NaN3 (0.1-3 mM) were submitted to oxidative stress with H2O2 (30-150 μM), to mimic conditions observed in neurodegenerative disorders. The effects of such treatment on a series of parameters useful in characterizing neuronal damage were investigated: (i) the basal release of glutamate, evaluated as (3)H-d-Aspartate efflux, was sharply, concentration-dependently, increased; (ii) the phosphorylation status of intracellular markers known to be involved in the neurodegenerative processes, in particular in Alzheimer disease: tau and GSK3β were increased, as well as the protein level of β-secretase (BACE1) and p35/25 evaluated by Western blotting, while (iii) the cell metabolic activity, measured with the MTT method, was reduced, in a concentration- and time-dependent manner. The latter effect, as well as tau hyperphosphorylation, was prevented both by a mixture of antioxidant drugs (100 μM ascorbic acid, 10 μM trolox, 100 μM glutathione) and by the anti-Alzheimer drug, memantine, 20 μM. PubMed:23722080

Appears in Networks:
Annotations
Uberon
cerebral cortex

a(CHEBI:"hydrogen peroxide") positiveCorrelation composite(a(CHEBI:"hydrogen peroxide"), a(CHEBI:"sodium azide")) View Subject | View Object

Primary cortical neurons exposed to the mitochondrial toxin NaN3 (0.1-3 mM) were submitted to oxidative stress with H2O2 (30-150 μM), to mimic conditions observed in neurodegenerative disorders. The effects of such treatment on a series of parameters useful in characterizing neuronal damage were investigated: (i) the basal release of glutamate, evaluated as (3)H-d-Aspartate efflux, was sharply, concentration-dependently, increased; (ii) the phosphorylation status of intracellular markers known to be involved in the neurodegenerative processes, in particular in Alzheimer disease: tau and GSK3β were increased, as well as the protein level of β-secretase (BACE1) and p35/25 evaluated by Western blotting, while (iii) the cell metabolic activity, measured with the MTT method, was reduced, in a concentration- and time-dependent manner. The latter effect, as well as tau hyperphosphorylation, was prevented both by a mixture of antioxidant drugs (100 μM ascorbic acid, 10 μM trolox, 100 μM glutathione) and by the anti-Alzheimer drug, memantine, 20 μM. PubMed:23722080

Appears in Networks:
Annotations
Uberon
cerebral cortex

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.