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bp(GO:"cell death")

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Entity

Name
cell death
Namespace
go
Namespace Version
20181221
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/73688d6dc24e309fca59a1340dc9ee971e9f3baa/external/go-names.belns

Appears in Networks 20

APP processing in Alzheimer's disease v1.0.1

APP processing in Alzheimer's disease

Proteolytic processing of Alzeimer's beta-amyloid precursor protein v1.0.1

albuquerque2009 v1.0.0

This file encodes the article Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function by Albuquerque et al, 2009

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

Activation of M1 and M4 muscarinic receptors as potential treatments for Alzheimer's disease and schizophrenia. v1.0.0

This file encodes the article Activation of M1 and M4 muscarinic receptors as potential treatments for Alzheimer’s disease and schizophrenia by Choi et al, 2014

M1 muscarinic acetylcholine receptor in Alzheimer’s disease v1.0.0

This file encodes the article M1 muscarinic acetylcholine receptor in Alzheimer’s disease by Jiang et al, 2014

The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0

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

Neuronal uptake and propagation of a rare phosphorylated high-molecular-weight tau derived from Alzheimer’s disease brain v1.0.1

The role of inflammasome in Alzheimer’s disease v1.0.3

Assembly and structure of protein phosphatase 2A v1.0.0

Alzheimer’s disease and the autophagic-lysosomal system v1.0.0

Molecular Chaperone Functions in Protein Folding and Proteostasis v1.0.0

Autophagy and the ubiquitin-proteasome system: collaborators in neuroprotection v1.0.0

Molecular chaperones and proteostasis regulation during redox imbalance v1.0.0

Extracellular low-n oligomers of tau cause selective synaptotoxicity without affecting cell viability v1.0.0

Carboxy terminus heat shock protein 70 interacting protein reduces tau-associated degenerative changes v1.0.0

Significance of NF-κB as a pivotal therapeutic target in the neurodegenerative pathologies of Alzheimer's disease and multiple sclerosis v1.0.0

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 44

a(CHEBI:"amyloid-beta") increases bp(GO:"cell death") View Subject | View Object

Picomolar levels of Abeta can also rescue neuronal cell death induced by inhibition of Abeta generation (by exposure to inhibitors of beta- or gamma-scretases) [160], possibly through regulating the potassium ion channel expression, hence affecting neuronal excitability [161] PubMed:21214928

Appears in Networks:
Annotations
MeSH
Endosomes
Confidence
Low
MeSH
Hippocampus
MeSH
Down Syndrome

p(HBP:HBP00071) increases bp(GO:"cell death") View Subject | View Object

Many studies have documented that AICD is cytotoxic and that over-expressing different AICDs (C31, C57, C59) in Hela, H4, N2a or PC12 cell lines, as well as neuronal cell lines, induces cell death (Lu et al. 2000) PubMed:22122372

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons

p(HGNC:PTGS2, loc(MESH:Neurons)) regulates bp(GO:"cell death") View Subject | View Object

In the brain, however, Cox2 is constitutively expressed by neurons (212, 512), participates in modulating synaptic plasticity (53, 464), and conditionally can either inhibit or promote cell death (74, 85, 237, 322, 451). PubMed:19126755

Appears in Networks:
Annotations
MeSH
Brain
Text Location
Review

a(CHEBI:thapsigargin) increases bp(GO:"cell death") View Subject | View Object

Nicotine protects SH-SY5Y cells from cell death induced by thapsigargin, an inhibitor of the sarcoplasmic-reticulum calcium pump (Arias et al., 2004). PubMed:19293145

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

a(MESH:Serum) decreases bp(GO:"cell death") 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

act(p(HGNC:CHRNA7)) decreases bp(GO:"cell death") 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

path(MESH:"Plaque, Amyloid") increases bp(GO:"cell death") View Subject | View Object

The popular amyloid cascade hypothesis posits that the gradual build-up of Abeta plaques leads to neuronal inflammation, dysfunction, and, eventually, cell death. The two brain regions most critically affected by this degeneration are the cortex and hippocampus, both of which are involved in cognition, learning, and memory. PubMed:24511233

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

p(HGNC:AIMP2) increases bp(GO:"cell death") View Subject | View Object

In the dopamine-producing neuroblastoma cell line SH-SY5Y, Parkin rescued the cells from p38-induced cell death PubMed:14556719

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

act(p(HGNC:CHRM1)) decreases bp(GO:"cell death") View Subject | View Object

Activation of M1 mAChR also protects against apoptotic factors in human neuroblastoma SH-SY5Y cells, such as DNA damage, oxidative stress, caspase activation, and mitochondrial impairment[83]. In addition, apoptosis induced by serum deprivation is blocked by M1 mAChR activation in a phosphoinositide 3-kinase- and MAPK/ERKindependent manner PubMed:24590577

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a(CHEBI:lactacystin) increases bp(GO:"cell death") View Subject | View Object

It has been shown that Abeta can be degraded by the proteasome in cultured neurons and astrocytes, and reatment with the proteasome inhibitor lactacystin decreased viability of cells exposed to Abeta (Lopez Salon et al., 2003). PubMed:14556719

Appears in Networks:
Annotations
Cell Ontology (CL)
astrocyte
Cell Ontology (CL)
neuron

bp(GO:"response to unfolded protein") increases bp(GO:"cell death") View Subject | View Object

It then aggregates, and the insoluble protein elicits cell death via the Unfolded Protein Response (UPR). PubMed:14556719

Appears in Networks:

p(HGNC:PRKN) decreases bp(GO:"cell death") View Subject | View Object

In the dopamine-producing neuroblastoma cell line SH-SY5Y, Parkin rescued the cells from p38-induced cell death PubMed:14556719

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

composite(a(CHEBI:cystamine), p(HGNC:AR, var("?"))) decreases bp(GO:"cell death") View Subject | View Object

Administration of cystamine, a transglutaminase inhibitor, can reduce aggregate formation and death in cells expressing atrophin-1 (DRPLA model) (Igarashi et al., 1998) and in cells expressing mutant androgen receptor (SBMA model) (Mandrusiak et al., 2003). PubMed:14556719

Appears in Networks:

composite(a(CHEBI:cystamine), p(HGNC:ATN1)) decreases bp(GO:"cell death") View Subject | View Object

Administration of cystamine, a transglutaminase inhibitor, can reduce aggregate formation and death in cells expressing atrophin-1 (DRPLA model) (Igarashi et al., 1998) and in cells expressing mutant androgen receptor (SBMA model) (Mandrusiak et al., 2003). PubMed:14556719

Appears in Networks:

composite(a(CHEBI:lactacystin), p(HGNC:SOD1, var("?"))) increases bp(GO:"cell death") View Subject | View Object

Thus, exposure to lactacystin resulted in increased cell death in human cell lines expressing mutant SOD1 (Aquilano et al., 2003; Hyun et al., 2003). PubMed:14556719

Appears in Networks:

p(HGNC:SOD1, var("?")) increases bp(GO:"cell death") View Subject | View Object

Similarly, overexpression of the putative SOD1 E3 ligase dorfin can inhibit cell death induced by the mutant protein (Niwa et al., 2002), presumably by promoting its removal via the UPS. PubMed:14556719

Appears in Networks:

p(FPLX:HSPA) increases bp(GO:"cell death") View Subject | View Object

Overexpression of the chaperone HSP70 has been found to reduce aggregate formation and death in nonneuronal cultured cells expressing mutant SOD1 (Bruening et al.,1999). PubMed:14556719

Appears in Networks:

p(HGNC:CDC34, var("?")) increases bp(GO:"cell death") View Subject | View Object

Tentative support for this idea was obtained in a cell model of HD, where expression of a dominant-negative variant of the E2 Cdc34p decreased the formation of intranuclear inclusions but increased the likelihood of cell death (Saudou et al., 1998). PubMed:14556719

Appears in Networks:
Annotations
MeSH
Huntington Disease

p(HGNC:GPR37) positiveCorrelation bp(GO:"cell death") View Subject | View Object

It then aggregates, and the insoluble protein elicits cell death via the Unfolded Protein Response (UPR). PubMed:14556719

Appears in Networks:

p(HGNC:RNF19A) decreases bp(GO:"cell death") View Subject | View Object

Similarly, overexpression of the putative SOD1 E3 ligase dorfin can inhibit cell death induced by the mutant protein (Niwa et al., 2002), presumably by promoting its removal via the UPS. PubMed:14556719

Appears in Networks:

act(p(HGNC:UBE3A)) decreases bp(GO:"cell death") View Subject | View Object

Interestingly, the expression of the inactive E3 increased the number of the dying Purkinje cells PubMed:14556719

Appears in Networks:
Annotations
Cell Ontology (CL)
Purkinje cell

a(GO:"neurofibrillary tangle") increases bp(GO:"cell death") View Subject | View Object

Tau-containing neurofibrillary tangle (NFT) accumulation is the closest correlate with cognitive decline and cell loss (Arriagada et al., 1992), yet mechanisms mediating tau toxicity are poorly understood PubMed:30126037

Appears in Networks:
Annotations
Confidence
High

a(GO:"neurofibrillary tangle") decreases bp(GO:"cell death") 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

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

p(HGNC:MAPT) increases bp(GO:"cell death") View Subject | View Object

While evidence has linked FTD with parkinsonism in patients to tau mutations on chromosome 17 (FTDP-17), implying that tau dysfunction alone can cause neurodegeneration (Reed et al., 2001), studies in animal models have shown that overexpression of tau can lead to cell death (Lee et al., 2001; Tanemura et al., 2001, 2002; Tatebayashi et al., 2002) and exhibit behavioral abnormalities and synaptic dysfunction without the presence of NFTs (Wittmann et al., 2001; Andorfer et al., 2003; Santacruz et al., 2005; Spires et al., 2006; Berger et al., 2007; Yoshiyama et al., 2007; Cowan et al., 2010) PubMed:28420982

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Cerebral Cortex

a(HBP:HBP00006) causesNoChange bp(GO:"cell death") View Subject | View Object

There was no difference in cell viability between tau-aggregate positive and negative cells for up to 4 days (Supplementary Fig. 10). PubMed:26458742

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain

path(MESH:"Brain Injuries, Traumatic") increases bp(GO:"cell death") View Subject | View Object

In human astrocytes, ATP released from damaged or dying cells after traumatic brain injury activates the NLRP2 inflammasome, leading to the maturation of both IL-1β and IL-18 (Minkiewicz et al., 2013) PubMed:24561250

Appears in Networks:
Annotations
Cell Ontology (CL)
astrocyte
Confidence
Medium
NeuroMMSigDB
Interleukin signaling subgraph

complex(GO:"protein phosphatase type 2A complex") regulates bp(GO:"cell death") View Subject | View Object

PP2A plays a critical role in cellular physiology including cell cycle regulation, cell proliferation and death, development, cytoskeleton dynamics, cell mobility, and regulation of multiple signal transduction pathways PubMed:19277525

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a(HBP:"alpha-synuclein oligomers") increases bp(GO:"cell death") View Subject | View Object

Misfolded α-synuclein proteins form insoluble oligomers, which in turn lead to the cascade of pathogenic neurotoxicity-induced responses such as neuroinflammation and cell death [55] PubMed:29758300

Appears in Networks:

composite(a(CHEBI:sirolimus), p(HGNC:MAPT, var("p.Ala152Thr"))) increases bp(GO:"cell death") View Subject | View Object

However, in another study, iPSC-derived tau A152T and MAPT IVS 10+16 (a tau splice mutant) cortical neurons had increased cell death in response to rapamycin treatment, although basal cell death was ∼10 times higher in these tau mutants relative to controls, making interpretation of the work difficult [134]. PubMed:29758300

Appears in Networks:

bp(HBP:Proteostasis) negativeCorrelation bp(GO:"cell death") View Subject | View Object

Additionally, PN regulation is integrated with pathways involved in inflam- mation, response to oxidative stress, caloric restriction/starvation, and longevity. PubMed:23746257

Appears in Networks:

a(GO:aggresome) negativeCorrelation bp(GO:"cell death") View Subject | View Object

It has been inferred that aggresome formation in vitro is a cytoprotective response in cultured cells since their formation correlates inversely with cell death, whereas interventions that block aggresome formation enhance cytotoxicity and slow the rate of turnover of misfolded proteins [27,64,70–72] PubMed:18930136

Appears in Networks:

bp(GO:autophagy) regulates bp(GO:"cell death") View Subject | View Object

Recent advances have demonstrated that autophagy also serves a surprisingly diverse array of additional functions, including organelle clearance, antigen presentation, elimination of microbes, as well as regulation of development and cell death [9]. PubMed:18930136

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bp(GO:"response to endoplasmic reticulum stress") decreases bp(GO:"cell death") View Subject | View Object

The three sensors of ER proteotoxic stress facilitate contra- dictory responses since they either promote cell survival by decreasing the misfolded protein and/or oxidative load, or, if UPR fails, they promote the activation of apoptotic pathways that eventually result in cell death [57]. PubMed:24563850

Appears in Networks:

bp(GO:"response to endoplasmic reticulum stress") increases bp(GO:"cell death") View Subject | View Object

The three sensors of ER proteotoxic stress facilitate contra- dictory responses since they either promote cell survival by decreasing the misfolded protein and/or oxidative load, or, if UPR fails, they promote the activation of apoptotic pathways that eventually result in cell death [57]. PubMed:24563850

Appears in Networks:

a(HBP:"Tau aggregates") causesNoChange bp(GO:"cell death") View Subject | View Object

In our hands, these aggregated tau species formed in different conditions did not show any significant release of LDH when applied on the differentiated SH-SY5Y cells (Supplementary Fig. 8A), and they did not show a significant reduction in cell viability by the MTTassay (Supplementary Fig. 8B). PubMed:28528849

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

p(HBP:"Tau oligomers", var("p.Lys280del")) increases bp(GO:"cell death") View Subject | View Object

To address this question, we first applied the oligomers directly after the purification of the protein eluting from the Butyl FF 16/ 10 column (without buffer exchange; 1, 5, and 10 mM) to SHSY5Y cells and observed a variety of toxic effects, including pronounced reduction in the cell viability (by MTT assay, Fig. 3A), increase in apoptotic cells (by Hoechst staining, Supplementary Fig. 4A), loss of mitochondrial membrane potential (by JC1 assay, Supplementary Fig. 4B), caspase 3/7 activation (Supplementary Fig. 4C-D), and cytochrome-c release (Supplementary Fig. 4), within 5 hours of incubation. PubMed:28528849

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

p(HBP:"Tau oligomers", var("p.Lys280del")) causesNoChange bp(GO:"cell death") View Subject | View Object

Consistent with this, NeuN staining of the slices fixed after 48 hours of treatment with TauRDΔK oligomers revealed no reduction in the neuronal number in all regions of the hippocampus (CA1, CA3, and DG) (Fig. 3C and D, Supplementary Fig. 7), confirming that TauRDΔK oligomers do not cause cell death in the OHSC model as well. PubMed:28528849

Appears in Networks:
Annotations
MeSH
CA1 Region, Hippocampal
MeSH
CA2 Region, Hippocampal
MeSH
CA3 Region, Hippocampal

p(HGNC:STUB1) causesNoChange bp(GO:"cell death") View Subject | View Object

Toxicity assays revealed that neither CHIP nor any of the tau constructs caused cell death compared to the control GFP vector (Supplementary Fig. 1). PubMed:25374103

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p(HBP:"Tau C3") causesNoChange bp(GO:"cell death") View Subject | View Object

Toxicity assays revealed that neither CHIP nor any of the tau constructs caused cell death compared to the control GFP vector (Supplementary Fig. 1). PubMed:25374103

Appears in Networks:

p(HBP:"Tau isoform F (441 aa)") causesNoChange bp(GO:"cell death") View Subject | View Object

Toxicity assays revealed that neither CHIP nor any of the tau constructs caused cell death compared to the control GFP vector (Supplementary Fig. 1). PubMed:25374103

Appears in Networks:

p(HBP:"4R tau", var("p.Lys280del")) causesNoChange bp(GO:"cell death") View Subject | View Object

Toxicity assays revealed that neither CHIP nor any of the tau constructs caused cell death compared to the control GFP vector (Supplementary Fig. 1). PubMed:25374103

Appears in Networks:

a(CHEBI:"amyloid-beta polypeptide 42") regulates bp(GO:"cell death") View Subject | View Object

Exposure of primary neuronal cells or post-mitotic neurons to Aβ1-42 peptide has been shown to strongly activate the p50:p65 dimers and mediate neuronal cell death (Fig 1) PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neurons
MeSH
Alzheimer Disease

a(CHEBI:lipopolysaccharide) increases bp(GO:"cell death") View Subject | View Object

Due to these properties, LPS can easily be incorporated into the membrane of (red blood) cells, alter their membrane properties, and thus promote cell death [123, 124]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Sepsis
Text Location
Review

p(MGI:Eif2ak1) negativeCorrelation bp(GO:"cell death") View Subject | View Object

Moreover, in the current study, we identified a crucial role of Hri in protecting erythroid precursors during differentiation by promoting terminal maturation including enucleation, preventing cell death, and increasing iron availability for erythropoiesis. PubMed:25411909

Appears in Networks:
Annotations
Cell Ontology (CL)
erythroid progenitor cell
MeSH
Spleen
Text Location
Discussion

Out-Edges 5

bp(GO:"cell death") positiveCorrelation p(HGNC:GPR37) View Subject | View Object

It then aggregates, and the insoluble protein elicits cell death via the Unfolded Protein Response (UPR). PubMed:14556719

Appears in Networks:

bp(GO:"cell death") increases sec(a(CHEBI:ATP)) View Subject | View Object

In human astrocytes, ATP released from damaged or dying cells after traumatic brain injury activates the NLRP2 inflammasome, leading to the maturation of both IL-1β and IL-18 (Minkiewicz et al., 2013) PubMed:24561250

Appears in Networks:
Annotations
Cell Ontology (CL)
astrocyte
Confidence
Medium
NeuroMMSigDB
Interleukin signaling subgraph

bp(GO:"cell death") negativeCorrelation bp(HBP:Proteostasis) View Subject | View Object

Additionally, PN regulation is integrated with pathways involved in inflam- mation, response to oxidative stress, caloric restriction/starvation, and longevity. PubMed:23746257

Appears in Networks:

bp(GO:"cell death") negativeCorrelation a(GO:aggresome) View Subject | View Object

It has been inferred that aggresome formation in vitro is a cytoprotective response in cultured cells since their formation correlates inversely with cell death, whereas interventions that block aggresome formation enhance cytotoxicity and slow the rate of turnover of misfolded proteins [27,64,70–72] PubMed:18930136

Appears in Networks:

bp(GO:"cell death") negativeCorrelation p(MGI:Eif2ak1) View Subject | View Object

Moreover, in the current study, we identified a crucial role of Hri in protecting erythroid precursors during differentiation by promoting terminal maturation including enucleation, preventing cell death, and increasing iron availability for erythropoiesis. PubMed:25411909

Appears in Networks:
Annotations
Cell Ontology (CL)
erythroid progenitor cell
MeSH
Spleen
Text Location
Discussion

About

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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.