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bp(MESH:"Cell Survival")

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Entity

Name
Cell Survival
Namespace
mesh
Namespace Version
20181007
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/8ccfed235e418e4c8aa576f9a5ef0f838e794c7f/external/mesh-names.belns

Appears in Networks 7

Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment v1.0.1

Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system v1.0.0

This document contains the curation of the review article Nicotinic receptors: allosteric transitions and therapeutic targets in the nervous system by Taly et al. 2009

Neuronal and Extraneuronal Nicotinic Acetylcholine Receptors. v1.0.0

Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers v1.0.0

This document contains the bel code for the Article Alzheimer’s disease-type neuronal tau hyperphosphorylation induced by Abeta oligomers by De Felice et al

Tau protein aggregation is associated with cellular senescence in the brain v1.0.0

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage v1.0.0

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage from Shafiei et al., 2017

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 18

act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) increases bp(MESH:"Cell Survival") View Subject | View Object

The explanation proposed by the authors is that alpha7 nAChR activation through nicotine binding could promote survival pathways and recover the synaptic damage caused by Abeta (Inestrosa et al., 2013) PubMed:25514383

Appears in Networks:
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MeSH
Alzheimer Disease

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) decreases bp(MESH:"Cell Survival") View Subject | View Object

On the other hand, an opposite effect was shown with Abeta-nAChR interaction being responsible for inhibition of survival pathways PubMed:25514383

Appears in Networks:

a(MESH:"3-(2,4-dimethoxybenzylidene)anabaseine") decreases bp(MESH:"Cell Survival") View Subject | View Object

As with nicotine, the weak alpha7 nAChR agonist GTS-21 is neuroprotective, specifically protecting against Abeta1–42-elicited neurotoxicity154. This effect is probably due to small, protracted increases in receptor-mediated Ca2+ influx. importantly, high concentrations of GTS-21 reduced cell survival, underlining the possible risk of over-stimulation152 PubMed:19721446

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Text Location
Review

a(MESH:Acetylcholine) association bp(MESH:"Cell Survival") View Subject | View Object

but ACh is also released by non-neuronal tissues where it is involved in cell-to-cell communication, and con- trols essential functions such as cell proliferation, adhesion, migration, secretion, survival and apoptosis, in an autocrine, paracrine or juxtacrine manner PubMed:28901280

Appears in Networks:

p(HGNC:CHRNA7) regulates bp(MESH:"Cell Survival") View Subject | View Object

α7-containing receptors are expressed in neurons and non-excitable cells in order to mediate pro-proliferative, sur- vival and anti-inflammatory signalling. PubMed:28901280

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MeSH
GABAergic Neurons

a(HBP:"amyloid-beta derived diffusible ligands") decreases bp(MESH:"Cell Survival") View Subject | View Object

At longer incubation times (48 and 96 h) ADDLs caused a progressive decrease in MTT reduction (Fig. 1B), which can be due to altered trafficking (Liu et al., 1998) as well as cell death. PubMed:17403556

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Text Location
Results

a(GO:"neurofibrillary tangle") increases bp(MESH:"Cell Survival") View Subject | View Object

NFT containing neurons upregulated genes involved in cell survival and viability, inflammation, cell cycle progression and molecular transport and downregulated apoptosis, necrosis and cell death pathways (Figure 1a). NFkB, a pro-survival master transcriptional regulator of inflammation, was the highest predicted upstream regulator of the NFT-gene expression profile. In agreement with inflammatory activation, other predicted upstream regulators included IFNG, TNF, TLR4, IL1B and CXCL1 (Figure 1b) PubMed:30126037

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Annotations
Confidence
Medium
MeSH
Neurons
MeSH
Alzheimer Disease

bp(GO:"cellular senescence") increases bp(MESH:"Cell Survival") View Subject | View Object

Transcriptomic analyses of NFT-containing neurons microdissected from postmortem AD brain revealed an expression profile consistent with cellular senescence. This complex stress response induces aberrant cell cycle activity, adaptations to maintain survival, cellular remodeling, and metabolic dysfunction PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Alzheimer Disease

bp(GO:"cellular senescence") increases bp(MESH:"Cell Survival") View Subject | View Object

This complex stress response induces a near permanent cell cycle arrest, adaptations to maintain survival, cellular remodeling, metabolic dysfunction and disruption to surrounding tissue to the secretion of toxic molecules (Childs et al., 2016) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Brain
MeSH
Alzheimer Disease

bp(GO:"cellular senescence") association bp(MESH:"Cell Survival") View Subject | View Object

NFkB regulates the pro-survival, pro-inflammatory SASP gene expression profile characteristic of cellular senescence (Salminen & Kaarniranta, 2011) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Neurons
MeSH
Alzheimer Disease

act(p(MGI:Nfkb1)) increases bp(MESH:"Cell Survival") View Subject | View Object

NFkB regulates the pro-survival, pro-inflammatory SASP gene expression profile characteristic of cellular senescence (Salminen & Kaarniranta, 2011) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Neurons
MeSH
Alzheimer Disease

a(HBP:"Tau oligomers") decreases bp(MESH:"Cell Survival") View Subject | View Object

Oligomeric tau intermediates decrease cell viability (Flach et al., 2012) PubMed:28420982

Appears in Networks:
Annotations
MeSH
Extracellular Space
Confidence
High
MeSH
Neurons
MeSH
Alzheimer Disease

a(CHEBI:heme) negativeCorrelation bp(MESH:"Cell Survival") View Subject | View Object

Whereas at the doses of 3, 4, and 5 μM, heme significantly reduced the viability of cells, which was in agreement with an earlier study [1]. PubMed:30324533

Appears in Networks:
Annotations
MeSH
Hematoma
Text Location
Results

a(MESH:"Glucose Oxidase") negativeCorrelation bp(MESH:"Cell Survival") View Subject | View Object

The result showed that cell viability loss in a GO dose-dependent manner, and 1.5 mU mL−1 GO induced approximately 15% cell death after 24 h of treatment (Fig. 2b). PubMed:30324533

Appears in Networks:
Annotations
MeSH
Hematoma
Text Location
Results

complex(a(CHEBI:"hydrogen peroxide"), a(CHEBI:heme)) negativeCorrelation bp(MESH:"Cell Survival") View Subject | View Object

As illustrated in Fig. 2d, the loss of viability by heme/H2O2 and heme/H2O2/NO2 − was approximately 53 ± 3.8% and 65 ± 4.5%, respectively, which further confirmed that NO2 − dramatically enhances heme/ H2O2 toxicity.This result is well consistent with previous reports [3, 13]. PubMed:30324533

Appears in Networks:
Annotations
MeSH
Hematoma
Text Location
Results

complex(a(CHEBI:"hydrogen peroxide"), a(CHEBI:heme), a(CHEBI:nitrite)) negativeCorrelation bp(MESH:"Cell Survival") View Subject | View Object

As illustrated in Fig. 2d, the loss of viability by heme/H2O2 and heme/H2O2/NO2 − was approximately 53 ± 3.8% and 65 ± 4.5%, respectively, which further confirmed that NO2 − dramatically enhances heme/ H2O2 toxicity.This result is well consistent with previous reports [3, 13]. PubMed:30324533

Appears in Networks:
Annotations
MeSH
Hematoma
Text Location
Results

p(HGNC:ALB) positiveCorrelation bp(MESH:"Cell Survival") View Subject | View Object

As shown in Fig. 2d, heme/H2O2/ NO2−-induced loss of cell viability was significantly attenuated by BSA or BSA-T pretreatment, and BSA was more effective than BSA-T. PubMed:30324533

Appears in Networks:
Annotations
MeSH
Hematoma
Text Location
Results

p(HGNC:ALB, pmod(Ph, Tyr)) positiveCorrelation bp(MESH:"Cell Survival") View Subject | View Object

As shown in Fig. 2d, heme/H2O2/ NO2−-induced loss of cell viability was significantly attenuated by BSA or BSA-T pretreatment, and BSA was more effective than BSA-T. PubMed:30324533

Appears in Networks:
Annotations
MeSH
Hematoma
Text Location
Results

Out-Edges 8

bp(MESH:"Cell Survival") association a(MESH:Acetylcholine) View Subject | View Object

but ACh is also released by non-neuronal tissues where it is involved in cell-to-cell communication, and con- trols essential functions such as cell proliferation, adhesion, migration, secretion, survival and apoptosis, in an autocrine, paracrine or juxtacrine manner PubMed:28901280

Appears in Networks:

bp(MESH:"Cell Survival") association bp(GO:"cellular senescence") View Subject | View Object

NFkB regulates the pro-survival, pro-inflammatory SASP gene expression profile characteristic of cellular senescence (Salminen & Kaarniranta, 2011) PubMed:30126037

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Neurons
MeSH
Alzheimer Disease

bp(MESH:"Cell Survival") negativeCorrelation a(CHEBI:heme) View Subject | View Object

Whereas at the doses of 3, 4, and 5 μM, heme significantly reduced the viability of cells, which was in agreement with an earlier study [1]. PubMed:30324533

Appears in Networks:
Annotations
MeSH
Hematoma
Text Location
Results

bp(MESH:"Cell Survival") negativeCorrelation a(MESH:"Glucose Oxidase") View Subject | View Object

The result showed that cell viability loss in a GO dose-dependent manner, and 1.5 mU mL−1 GO induced approximately 15% cell death after 24 h of treatment (Fig. 2b). PubMed:30324533

Appears in Networks:
Annotations
MeSH
Hematoma
Text Location
Results

bp(MESH:"Cell Survival") negativeCorrelation complex(a(CHEBI:"hydrogen peroxide"), a(CHEBI:heme)) View Subject | View Object

As illustrated in Fig. 2d, the loss of viability by heme/H2O2 and heme/H2O2/NO2 − was approximately 53 ± 3.8% and 65 ± 4.5%, respectively, which further confirmed that NO2 − dramatically enhances heme/ H2O2 toxicity.This result is well consistent with previous reports [3, 13]. PubMed:30324533

Appears in Networks:
Annotations
MeSH
Hematoma
Text Location
Results

bp(MESH:"Cell Survival") negativeCorrelation complex(a(CHEBI:"hydrogen peroxide"), a(CHEBI:heme), a(CHEBI:nitrite)) View Subject | View Object

As illustrated in Fig. 2d, the loss of viability by heme/H2O2 and heme/H2O2/NO2 − was approximately 53 ± 3.8% and 65 ± 4.5%, respectively, which further confirmed that NO2 − dramatically enhances heme/ H2O2 toxicity.This result is well consistent with previous reports [3, 13]. PubMed:30324533

Appears in Networks:
Annotations
MeSH
Hematoma
Text Location
Results

bp(MESH:"Cell Survival") positiveCorrelation p(HGNC:ALB) View Subject | View Object

As shown in Fig. 2d, heme/H2O2/ NO2−-induced loss of cell viability was significantly attenuated by BSA or BSA-T pretreatment, and BSA was more effective than BSA-T. PubMed:30324533

Appears in Networks:
Annotations
MeSH
Hematoma
Text Location
Results

bp(MESH:"Cell Survival") positiveCorrelation p(HGNC:ALB, pmod(Ph, Tyr)) View Subject | View Object

As shown in Fig. 2d, heme/H2O2/ NO2−-induced loss of cell viability was significantly attenuated by BSA or BSA-T pretreatment, and BSA was more effective than BSA-T. PubMed:30324533

Appears in Networks:
Annotations
MeSH
Hematoma
Text Location
Results

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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.