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bp(GO:"apoptotic process")

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

Appears in Networks 28

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

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

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

Chaperoning α7 neuronal nicotinic acetylcholine receptors v1.0.0

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

The Biology of Proteostasis in Aging and Disease v1.0.0

Alpha-synuclein oligomers: a new hope v1.0.0

Structural and functional properties of prefibrillar α-synuclein oligomers v1.0.0

MMP-9 and MMP-2 Contribute to Neuronal Cell Death in iPSC Models of Frontotemporal Dementia with MAPT Mutations v1.0.0

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

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

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Activation and regulation of the inflammasomes v1.0.0

Inflammasome Involvement in Alzheimer’s Disease v1.0.0

Amyloid-Binding Alcohol Dehydrogenase (ABAD) Inhibitors for the Treatment of Alzheimer’s Disease v1.0.0

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Protein phosphatase 2A dysfunction in Alzheimer’s disease v1.0.0

The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease 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

New insights into the role of microRNAs and long noncoding RNAs in most common neurodegenerative diseases v1.0.0

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

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Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease 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 94

a(HBP:HBP00071) increases bp(GO:"apoptotic process") View Subject | View Object

In addition, free AICD can induce apoptosis and may play a role in sensitizing neurons to toxic stimuli [133,134] PubMed:21214928

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Annotations
MeSH
Endosomes
Confidence
High
MeSH
Neurons

complex(p(HBP:HBP00071), p(HGNC:NAE1)) increases bp(GO:"apoptotic process") View Subject | View Object

APP-binding protein 1 reportedly interacts with AICD and activates the neddylation pathway (Chen 2004), further down-regulating the level of beta-catenin and potentially resulting in apoptosis PubMed:22122372

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Annotations
Confidence
High
MeSH
Neurons

act(p(HGNC:TP53)) increases bp(GO:"apoptotic process") View Subject | View Object

For example, P53 expression, as well as p53-mediated apoptosis, can be enhanced by AICD (Alves da Costa et al. 2006; Ozaki et al. 2006) PubMed:22122372

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Annotations
Confidence
Medium
MeSH
Neurons

act(a(CHEBI:"amyloid-beta")) increases bp(GO:"apoptotic process") View Subject | View Object

Thus, it seems that nAChRs may play a role in mediating Abeta toxicity through synergistic mechanisms; in addition to possible direct interactions (binding), nAChRs may also result in accelerated cell death through enhancing intracellular Abeta accumulation. PubMed:19293145

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a(CHEBI:nicotine) decreases bp(GO:"apoptotic process") View Subject | View Object

The AD therapeutic AChE inhibitors donepezil, galantamine, and tacrine increase BCL2 expression when applied to cultured neuronal cells (Arias et al., 2004; Takada-Takatori et al., 2006). In these cells, nicotine promotes cell survival and causes the phosphorylation of the proapoptotic protein Bcl2-associated X protein (BAX), through the PI3K/AKT pathway, reducing the movement of BAX from the cytosol to the mitochondria and inhibiting its apoptotic activity (Xin and Deng, 2005). PubMed:19293145

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MeSH
Neurons

a(CHEBI:nicotine) decreases bp(GO:"apoptotic process") 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

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Experimental Factor Ontology (EFO)
PC12

bp(GO:"ERK1 and ERK2 cascade") increases bp(GO:"apoptotic process") View Subject | View Object

Furthermore, nicotinic activation of ERK-1/2 promotes survival of cultured murine spinal cord neurons, and the blocking of ERK-1 prevents nicotine’s antiapoptotic action (Toborek et al., 2007). Likewise, the alpha7-specific agonist A-582941 induces phosphorylation of ERK-1/2 in PC12 cells and in mouse brain, and this is completely blocked by the mitogen-activated protein kinase 1 inhibitor SL327 (Bitner et al., 2007). PubMed:19293145

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p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits") association bp(GO:"apoptotic process") View Subject | View Object

Thus, it seems that nAChRs may play a role in mediating Abeta toxicity through synergistic mechanisms; in addition to possible direct interactions (binding), nAChRs may also result in accelerated cell death through enhancing intracellular Abeta accumulation. PubMed:19293145

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p(HGNC:FYN) decreases bp(GO:"apoptotic process") View Subject | View Object

In a microarray study comparing brains from patients with AD with control brains, FYN was found to be significantly upregulated in AD (Wang et al., 2003a). In this context, it is of interest that FYN has also been shown to activate the PI3K/AKT cascade, thereby inhibiting apoptosis (Tang et al., 2007). Indeed, FYN is required for phos- phorylation of phosphoinositide 3-kinase enhancer (PIKE), which itself regulates AKT (Fig. 3). PIKE binds to AKT and up-regulates its kinase a ctivity, thereby reducing apoptosis. Phosphorylation protects PIKE from caspase cleavage, hence FYN is antiapoptotic (Tang et al., 2007). PubMed:19293145

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act(p(FPLX:AKT)) decreases bp(GO:"apoptotic process") View Subject | View Object

In a microarray study comparing brains from patients with AD with control brains, FYN was found to be significantly upregulated in AD (Wang et al., 2003a). In this context, it is of interest that FYN has also been shown to activate the PI3K/AKT cascade, thereby inhibiting apoptosis (Tang et al., 2007). Indeed, FYN is required for phos- phorylation of phosphoinositide 3-kinase enhancer (PIKE), which itself regulates AKT (Fig. 3). PIKE binds to AKT and up-regulates its kinase a ctivity, thereby reducing apoptosis. Phosphorylation protects PIKE from caspase cleavage, hence FYN is antiapoptotic (Tang et al., 2007). PubMed:19293145

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complex(p(FPLX:AKT), p(HGNC:BAD)) regulates bp(GO:"apoptotic process") View Subject | View Object

AKT interacts with BAD to regulate apoptosis and, interestingly, also has many interacting partners in the insulin signaling pathway. Abeta increased activity of BAD, lowered the activity of the antiapoptotic protein BCL2, in rat hippocampal neurons in primary culture (Koriyama et al., 2003) and has been shown to be toxic to human neuroblastoma cells by increasing BAX activity and decreasing BCl-2 activity (Clementi et al., 2006). PubMed:19293145

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act(p(HGNC:MAPK1)) increases bp(GO:"apoptotic process") View Subject | View Object

Abeta initiates intracellular signaling cascades via nAChRs (Fig. 3), including the MAPK kinase signaling pathway, resulting in cell death. In hippocampal slices, Abeta activates ERK-2 isoforms of the ERK MAPK. This is blocked by alpha7 antagonists, suggesting that Abeta evokes the cascade through alpha7 nAChRs (Dineley et al., 2001). PubMed:19293145

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Annotations
MeSH
Hippocampus

act(p(FPLX:PI3K)) decreases bp(GO:"apoptotic process") View Subject | View Object

For instance, over-expressing PI3K in Drosophila melanogaster neurons in situ results in an increase in functional synapses as well as synaptic sprouting (Martín-Pen˜ a et al., 2006). Thus it is possible that nicotine’s activation of the PI3K pathway results in increased synaptic stability, and it would be of interest to explore this further in vertebrates. Thus, the evidence suggests that activation of nAChRs activates the PI3K/AKT pathway to favor antiapoptotic pathways and possibly induce synaptogenesis. PubMed:19293145

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tloc(p(HGNC:BAX), fromLoc(GO:cytosol), toLoc(GO:mitochondrion)) increases bp(GO:"apoptotic process") View Subject | View Object

The AD therapeutic AChE inhibitors donepezil, galantamine, and tacrine increase BCL2 expression when applied to cultured neuronal cells (Arias et al., 2004; Takada-Takatori et al., 2006). In these cells, nicotine promotes cell survival and causes the phosphorylation of the proapoptotic protein Bcl2-associated X protein (BAX), through the PI3K/AKT pathway, reducing the movement of BAX from the cytosol to the mitochondria and inhibiting its apoptotic activity (Xin and Deng, 2005). PubMed:19293145

Appears in Networks:
Annotations
MeSH
Neurons

act(p(HGNC:MYC)) increases bp(GO:"apoptotic process") View Subject | View Object

Application of nicotine to rat microglia results in the up-regulated expression of cyclooxygenase-2 and prostaglandin E2 (De Simone et al., 2005). Signaling pathways downstream to the MAPK pathway are similarly well placed to effect changes in gene expression. For example, alpha7-dependent activation of the MAPK pathway is known to activate c-Myc (Liu et al., 2007), a protooncogene whose transcription product sensitizes cells to pro-apoptotic stimuli. PubMed:19293145

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Cell Ontology (CL)
microglial cell

p(FPLX:AKT) regulates bp(GO:"apoptotic process") View Subject | View Object

Akt plays an important role in cell growth, proliferation and apoptosis. PubMed:23454242

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a(CHEBI:"pregnenolone sulfate") decreases bp(GO:"apoptotic process") View Subject | View Object

The treatment improved spatial memory and reduced apoptosis in CA1 pyramidal cells PubMed:25514383

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Annotations
MeSH
CA1 Region, Hippocampal
MeSH
Pyramidal Cells
MeSH
Alzheimer Disease

a(CHEBI:nicotine) decreases bp(GO:"apoptotic process") View Subject | View Object

Akt phosphorylation mediates the downstream activation of an antiapoptotic pathway, which is also activated by nicotine treatment (Kihara et al., 2001) PubMed:25514383

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a(CHEBI:simvastatin) decreases bp(GO:"apoptotic process") View Subject | View Object

In a study conducted by Zhi et al. (2014), this molecule was used to treat a mouse model obtained with injections of the peptide Aß25-35. Administration for 11 days of SV improved memory performance in the Morris water maze task and promoted survival of CA1 pyramidal cells. This effect was proposed to be promoted by alpha7 nAChRs, since it is blocked by MLA administration (Zhi et al., 2014) PubMed:25514383

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Annotations
MeSH
CA1 Region, Hippocampal
MeSH
Pyramidal Cells
MeSH
Alzheimer Disease

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") decreases bp(GO:"apoptotic process") View Subject | View Object

In a study conducted by Zhi et al. (2014), this molecule was used to treat a mouse model obtained with injections of the peptide Aß25-35. Administration for 11 days of SV improved memory performance in the Morris water maze task and promoted survival of CA1 pyramidal cells. This effect was proposed to be promoted by alpha7 nAChRs, since it is blocked by MLA administration (Zhi et al., 2014) PubMed:25514383

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Annotations
MeSH
CA1 Region, Hippocampal
MeSH
Pyramidal Cells
MeSH
Alzheimer Disease

p(FPLX:AKT, pmod(Ph)) decreases bp(GO:"apoptotic process") View Subject | View Object

Akt phosphorylation mediates the downstream activation of an antiapoptotic pathway, which is also activated by nicotine treatment (Kihara et al., 2001) PubMed:25514383

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p(HGNC:CHRNA7) decreases bp(GO:"apoptotic process") View Subject | View Object

During acute in- flammatory processes α7 AChRs attenuate renal failure induced by ische- mia/reperfusion by inhibiting pro-inflammatory cytokine expression, and subsequently decreasing cell apoptosis [180,201]. PubMed:22040696

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MeSH
Inflammation

p(HGNC:SNCA) increases bp(GO:"apoptotic process") View Subject | View Object

Overexpression of wild-type, but in particular mutant alphaSYN in many cell types but not in all, induces apoptosis or sensitizes the cells to toxic agents, including proteasome inhibitors (see, for example, Lee et al.,2001a). PubMed:14556719

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p(HGNC:HTT, var("?")) increases bp(GO:"apoptotic process") View Subject | View Object

A study in cultured mouse neuroblastoma cells showed that N-terminal mutant Huntingtin inhibited the 20S proteasome catalytic activity, in turn causing impaired proteasomal degradation of p53, subsequent loss of mitochondrial membrane potential, release of cytochrome c, caspase activation, and apoptosis (Jana et al., 2001) (Figure 2). PubMed:14556719

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p(HGNC:SNCA, var("?")) increases bp(GO:"apoptotic process") View Subject | View Object

Overexpression of wild-type, but in particular mutant alphaSYN in many cell types but not in all, induces apoptosis or sensitizes the cells to toxic agents, including proteasome inhibitors (see, for example, Lee et al.,2001a). PubMed:14556719

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p(HGNC:DDIT3) increases bp(GO:"apoptotic process") View Subject | View Object

Under these conditions, ATF4 mRNA is preferentially translated, leading to selective expression of the proapoptotic TF CHOP, which elicits apoptosis if ER stress is not resolved, presumably to ensure that irreversibly damaged cells are removed from the population. PubMed:25784053

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a(HBP:HBP00092) causesNoChange bp(GO:"apoptotic process") View Subject | View Object

In contrast, a-syn 30–110 that forms fibrils at a fast rate, did not display toxicity, indicating that oligomers are indeed the toxic species leading to TH-neuron loss in vivo [162]. PubMed:28803412

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Annotations
Cell Ontology (CL)
neuron
Confidence
High

a(HBP:HBP00093) increases bp(GO:"apoptotic process") View Subject | View Object

In vitro formed a-syn oligomers ectopically applied to cell cultures or formed due to overexpression of a-syn induce cell death [20, 30, 109, 149], which has been recapitulated in vivo in several studies. PubMed:28803412

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Confidence
High

a(HBP:HBP00093) increases bp(GO:"apoptotic process") View Subject | View Object

In contrast, a-syn 30–110 that forms fibrils at a fast rate, did not display toxicity, indicating that oligomers are indeed the toxic species leading to TH-neuron loss in vivo [162]. PubMed:28803412

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Annotations
Cell Ontology (CL)
neuron
Confidence
High

a(HBP:HBP00094) decreases bp(GO:"apoptotic process") View Subject | View Object

Prabhudesai et al. showed that this molecule is able to inhibit the aggregation of a-syn in vitro and in a zebrafish model expressing human wild-type a-syn in neurons where CLR01 reduced apoptosis and improved embryo survival [127]. PubMed:28803412

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Annotations
Cell Ontology (CL)
neuron
Confidence
High
MeSH
Brain
MeSH
Cerebrospinal Fluid
MeSH
Serum

a(HBP:HBP00092) increases bp(GO:"apoptotic process") View Subject | View Object

α -syn fibrils revealed to be highly toxic to cells at all the concentrations we tested, spanning 1 to 0.01 nM (53.4 ± 4% inhibition of MTT reduction at 0.01 nM, i.e. 0.1 μM equivalent monomer concentration) whereas α -syn oligomers only slightly impaired cell viability (23.9 ± 6% inhibition of MTT reduction at 300 nM, i.e. 10 μM initial monomer concentration) (Fig. 3c). PubMed:27075649

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Annotations
MeSH
Intracellular Space
Cell Ontology (CL)
neuron
Confidence
High
MeSH
Lewy Bodies

a(HBP:HBP00093) increases bp(GO:"apoptotic process") View Subject | View Object

α -syn fibrils revealed to be highly toxic to cells at all the concentrations we tested, spanning 1 to 0.01 nM (53.4 ± 4% inhibition of MTT reduction at 0.01 nM, i.e. 0.1 μM equivalent monomer concentration) whereas α -syn oligomers only slightly impaired cell viability (23.9 ± 6% inhibition of MTT reduction at 300 nM, i.e. 10 μM initial monomer concentration) (Fig. 3c). PubMed:27075649

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Annotations
MeSH
Intracellular Space
Cell Ontology (CL)
neuron
Confidence
High
MeSH
Lewy Bodies

a(CHEBI:staurosporine) increases bp(GO:"apoptotic process") View Subject | View Object

We treated these neurons with staurosporine, a broad-spectrum kinase inhibitor that induces apoptosis (Budd et al., 2000); rotenone, a complex inhibitor that induces mitochondrial dysfunction (Sherer et al., 2003); and rapamycin, an inhibitor of the mammalian target of the rapamycin (mTOR) signaling pathway with many downstream effects (Li et al., 2014) PubMed:27594586

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Annotations
MeSH
Extracellular Space
Confidence
High
MeSH
Cerebral Cortex
MeSH
Neurons
MeSH
Frontotemporal Dementia

a(CHEBI:Thrombin) increases bp(GO:"apoptotic process") View Subject | View Object

A recent study showed that thrombin is elevated in microvessels isolated from AD brain compared to microvessels from control brain (33). Additionally, thrombin was present in the CSF of AD patients but not in that of controls (33). This is important, as thrombin can act as a neurotoxin by activating intracellular signaling cascades causing neurite retraction and stimulating apoptosis (34–36) PubMed:24027553

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Text Location
Review

a(CHEBI:Thrombin) increases bp(GO:"apoptotic process") View Subject | View Object

Thrombin may also be influencing tau pathology, as treatment of immortalized hippocampal neuronal cells (HT22 cells) with thrombin resulted in the formation of thioflavin-S positive tau aggregates within 24 h, followed by an increase in cell death at 72 h (37). PubMed:24027553

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Annotations
MeSH
Hippocampus
Text Location
Review

p(HBP:"Tau C3") increases bp(GO:"apoptotic process") View Subject | View Object

There may be reciprocity with the apoptosis pathway as activating caspase-3 by inducing apoptosis in cortical neuronal culture led to tau cleavage (22), and selectively expressing tauC3 led to apoptosis in NT2 and COS cells (21). This might represent a feed-forward loop of neurotoxicity. PubMed:24027553

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Text Location
Review

act(p(HGNC:CASP6)) increases bp(GO:"apoptotic process") View Subject | View Object

Caspase-6 was also shown to cleave the N-terminus of tau in vitro (24). Caspase-3, which is a key effector in the apoptotic cascade, cleaves tau predominantly at the C-terminal D421 site generating a fragment often referred to as tauC3 (22, 23). PubMed:24027553

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Text Location
Review

p(HGNC:MAPT, frag("?", "17kD")) association bp(GO:"apoptotic process") 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

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Annotations
Experimental Factor Ontology (EFO)
PC12
Text Location
Review

p(HGNC:MAPT, var("p.D421E")) decreases bp(GO:"apoptotic process") View Subject | View Object

Furthermore, expressing a cleavage resistant form of tau (D421E) protects cells from apoptotic cell death (22). Another potential mechanism of inducing caspase-3 cleavage of tau is the presence of Aβ peptides. TauC3 is formed in primary cortical neurons after treatment with Aβ (23). PubMed:24027553

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Text Location
Review

a(GO:"neurofibrillary tangle") decreases bp(GO:"apoptotic process") 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

a(CHEBI:glyceraldehyde) increases bp(GO:"apoptotic process") View Subject | View Object

A relationship has recently been reported between the expression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and apoptotic events14. Real-time RT-PCR experiments showed that the expression of GAPDH was significantly increased by the addition of GA (Fig. 2a). These results suggested that GA caused cell toxicity concomitant with increases in the gene expression of GAPDH in SH-SY5Y cells. PubMed:26304819

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p(HBP:"Tau aggregates") increases bp(GO:"apoptotic process") View Subject | View Object

D-ribosylated Tau aggregates were highly toxic to SHSY5Y cells and resulted in both apoptosis and necrosis PubMed:19517062

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bp(MESH:"Oxidative Stress") causesNoChange bp(GO:"apoptotic process") View Subject | View Object

Only middle-aged Tet-mev-1 mice showed JNK/MARK activation and Ca2+ overload, particularly in astrocytes with decreased hippocampal GFAP and S100ß, but without pathological features such as apoptosis, amyloidosis, and lactic acidosis in neurons and astrocytes. This led to decreasing levels of glial fibrillary acidic protein and S100β in the hippocampal area. PubMed:27623715

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Annotations
Uberon
hippocampal formation
Cell Ontology (CL)
astrocyte
Cell Ontology (CL)
neuron

p(HGNC:MAPT, pmod(Ph, Ser, 396)) negativeCorrelation bp(GO:"apoptotic process") View Subject | View Object

These data suggest that tau hyperphosphorylation at Thr231, Ser262, and Ser396 by DAPK1 renders the cells more resistant to the kinase-induced apoptotic cell death, providing new insights into the tau-involved apoptotic abortion in the course of chronic neurodegeneration. PubMed:23948915

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act(p(HGNC:DAPK1)) increases bp(GO:"apoptotic process") View Subject | View Object

In this report, we describe a novel mechanism of action determined by the JunD component of AP-1, a factor enhancing cell survival in v-Src-transformed cells. We show that the loss of JunD results in the aberrant activation of a genetic program leading to cell death. This program requires the activation of the tumor suppressor death-associated protein kinase 1 (DAPK1). Since DAPK1 is phosphorylated and inhibited by v-Src, these results highlight the importance of this kinase and the multiple mechanisms controlled by v-Src to antagonize the tumor suppressor function of DAPK1. PubMed:27795443

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act(p(HGNC:JUND)) decreases bp(GO:"apoptotic process") View Subject | View Object

In this report, we describe a novel mechanism of action determined by the JunD component of AP-1, a factor enhancing cell survival in v-Src-transformed cells. We show that the loss of JunD results in the aberrant activation of a genetic program leading to cell death. This program requires the activation of the tumor suppressor death-associated protein kinase 1 (DAPK1). Since DAPK1 is phosphorylated and inhibited by v-Src, these results highlight the importance of this kinase and the multiple mechanisms controlled by v-Src to antagonize the tumor suppressor function of DAPK1. PubMed:27795443

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p(HGNC:MAPT, pmod(Ph, Ser, 262)) negativeCorrelation bp(GO:"apoptotic process") View Subject | View Object

These data suggest that tau hyperphosphorylation at Thr231, Ser262, and Ser396 by DAPK1 renders the cells more resistant to the kinase-induced apoptotic cell death, providing new insights into the tau-involved apoptotic abortion in the course of chronic neurodegeneration. PubMed:23948915

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p(HGNC:MAPT, pmod(Ph, Thr, 231)) negativeCorrelation bp(GO:"apoptotic process") View Subject | View Object

These data suggest that tau hyperphosphorylation at Thr231, Ser262, and Ser396 by DAPK1 renders the cells more resistant to the kinase-induced apoptotic cell death, providing new insights into the tau-involved apoptotic abortion in the course of chronic neurodegeneration. PubMed:23948915

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p(MGI:Itpkb) increases bp(GO:"apoptotic process") View Subject | View Object

We show here that ITPKB protein level was increased 3-fold in the cerebral cortex of most patients with Alzheimer's disease compared with control subjects, and accumulated in dystrophic neurites associated to amyloid plaques. In mouse Neuro-2a neuroblastoma cells, Itpkb overexpression was associated with increased cell apoptosis and increased β-secretase 1 activity leading to overproduction of amyloid-β peptides. In this cellular model, an inhibitor of mitogen-activated kinase kinases 1/2 completely prevented overproduction of amyloid-β peptides. Transgenic overexpression of ITPKB in mouse forebrain neurons was not sufficient to induce amyloid plaque formation or tau hyperphosphorylation. However, in the 5X familial Alzheimer's disease mouse model, neuronal ITPKB overexpression significantly increased extracellular signal-regulated kinases 1/2 activation and β-secretase 1 activity, resulting in exacerbated Alzheimer's disease pathology as shown by increased astrogliosis, amyloid-β40 peptide production and tau hyperphosphorylation. PubMed:24401760

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r(HGNC:GAPDH) association bp(GO:"apoptotic process") View Subject | View Object

A relationship has recently been reported between the expression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and apoptotic events14. Real-time RT-PCR experiments showed that the expression of GAPDH was significantly increased by the addition of GA (Fig. 2a). These results suggested that GA caused cell toxicity concomitant with increases in the gene expression of GAPDH in SH-SY5Y cells. PubMed:26304819

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bp(GO:autophagy) regulates bp(GO:"apoptotic process") View Subject | View Object

Furthermore, autophagy can regulate both apoptosis and inflammasome assembly, and, depending on the conditions, can be either pro- or anti-apoptotic104 PubMed:23702978

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Annotations
Confidence
High
MeSH
Extracellular Space
NeuroMMSigDB
Apoptosis signaling subgraph

act(p(HGNC:P2RX7)) increases bp(GO:"apoptotic process") View Subject | View Object

P2X7 activation is followed by a number of downstream events, including release of pro-inflammatory mediators, cell death, and proliferation. PubMed:27314526

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Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Apoptosis signaling subgraph
NeuroMMSigDB
Inflammatory response subgraph

complex(p(HGNC:APP), p(HGNC:HSD17B10)) increases bp(GO:"apoptotic process") View Subject | View Object

In another study, neurons from Tg mAPP/ABAD mice were shown to exhibit decreased activity of cyclooxygenase (COX) enzyme, spontaneous release of ROS, loss of mitochondrial membrane potential, a decrease in ATP production and release of cytochrome c from mitochondria with subsequent induction of caspase-3-like activity followed by apoptotic cell death. PubMed:30444369

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MeSH
Neurons

p(HGNC:BCL2) decreases bp(GO:"apoptotic process") View Subject | View Object

It enhances the expression of anti- apoptotic proteins, such as Bcl-2 and Bcl-xL, and down-regulates the expression of Bim, a pro-apoptotic factor, preventing programmed cell death. 90, 100 Estradiol also activates antioxidant systems to protect neuronal cells from apoptosis by upregulating the expression of manganese superoxide dismutase and glutathione peroxidase. 101 PubMed:30444369

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MeSH
Neurons

p(HGNC:BCL2L1) decreases bp(GO:"apoptotic process") View Subject | View Object

It enhances the expression of anti- apoptotic proteins, such as Bcl-2 and Bcl-xL, and down-regulates the expression of Bim, a pro-apoptotic factor, preventing programmed cell death. 90, 100 Estradiol also activates antioxidant systems to protect neuronal cells from apoptosis by upregulating the expression of manganese superoxide dismutase and glutathione peroxidase. 101 PubMed:30444369

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MeSH
Neurons

p(HGNC:BCL2L11) increases bp(GO:"apoptotic process") View Subject | View Object

It enhances the expression of anti- apoptotic proteins, such as Bcl-2 and Bcl-xL, and down-regulates the expression of Bim, a pro-apoptotic factor, preventing programmed cell death. 90, 100 Estradiol also activates antioxidant systems to protect neuronal cells from apoptosis by upregulating the expression of manganese superoxide dismutase and glutathione peroxidase. 101 PubMed:30444369

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MeSH
Neurons

bp(GO:phosphorylation) regulates bp(GO:"apoptotic process") View Subject | View Object

In a typical cell, the functions of nearly one-third of the proteins are regulated via phosphorylation and it controls various biological functions like cell division, growth and development, survival, proliferation, and apoptosis. PubMed:23454242

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p(FPLX:PPP2) regulates bp(GO:"apoptotic process") View Subject | View Object

PP2A is an important player in many cellular functions. It controls cell metabolism by regulating the activity of the enzymes involved in glycolysis, lipid metabolism and catecholamine synthesis [8]. It also regulates various biological processes such as the cell cycle (by mediating cdc2 kinase activation), DNA replication, transcription and translation, signal transduction, cell proliferation, cytoskeleton dynamics and cell mobility and apoptosis. It has also been shown to play a role in cell transformation and cancer [9-12]. PubMed:23454242

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p(FPLX:PPP2) regulates bp(GO:"apoptotic process") View Subject | View Object

Co-immunoprecipitation and in-vitro pull down assay using pro-lymphoid FL5.12 cells showed a direct association of the PP2A-B55 holoenzyme with Akt, which selectively regulates phosphorylation of Akt at Thr-308 and regulates cell proliferation and survival [58]. PubMed:23454242

Appears in Networks:

p(HGNC:BAD, pmod(Ph)) decreases bp(GO:"apoptotic process") View Subject | View Object

Phosphorylation of BAD suppresses, and its dephosphorylation by PP2A promotes pro-apoptotic activity [59]. Additionally, phosphorylation of Bcl-2 activates, and its dephosphorylation by PP2A suppresses anti- apoptotic activity. PubMed:23454242

Appears in Networks:

p(HGNC:BCL2, pmod(Ph)) decreases bp(GO:"apoptotic process") View Subject | View Object

Phosphorylation of BAD suppresses, and its dephosphorylation by PP2A promotes pro-apoptotic activity [59]. Additionally, phosphorylation of Bcl-2 activates, and its dephosphorylation by PP2A suppresses anti- apoptotic activity. PubMed:23454242

Appears in Networks:

act(p(HGNC:CDK5)) positiveCorrelation bp(GO:"apoptotic process") View Subject | View Object

Apart from affecting tau phosphorylation, abnormal activation of GSK3β, cdk5, and ERK has been linked to cytoskeletal abnormalities (microtubules, neurofilaments), alterations in amyloid precursor protein (APP) phosphorylation and processing, impairment of neurogenesis, alterations in synaptic plasticity and induction of apoptotic processes (Reviewed in Crews and Masliah, 2010; Medina and Avila, 2013, 2014). PubMed:24653673

Appears in Networks:

act(p(HGNC:GSK3B)) positiveCorrelation bp(GO:"apoptotic process") View Subject | View Object

Apart from affecting tau phosphorylation, abnormal activation of GSK3β, cdk5, and ERK has been linked to cytoskeletal abnormalities (microtubules, neurofilaments), alterations in amyloid precursor protein (APP) phosphorylation and processing, impairment of neurogenesis, alterations in synaptic plasticity and induction of apoptotic processes (Reviewed in Crews and Masliah, 2010; Medina and Avila, 2013, 2014). PubMed:24653673

Appears in Networks:

act(p(FPLX:ERK)) positiveCorrelation bp(GO:"apoptotic process") View Subject | View Object

Apart from affecting tau phosphorylation, abnormal activation of GSK3β, cdk5, and ERK has been linked to cytoskeletal abnormalities (microtubules, neurofilaments), alterations in amyloid precursor protein (APP) phosphorylation and processing, impairment of neurogenesis, alterations in synaptic plasticity and induction of apoptotic processes (Reviewed in Crews and Masliah, 2010; Medina and Avila, 2013, 2014). PubMed:24653673

Appears in Networks:

sec(a(MESH:Cathepsins)) increases bp(GO:"apoptotic process") View Subject | View Object

Cataclysmic disruption of lysosomal membranes releases hydrolases that act as both the trigger and executioner in rapid necrosis (Syntichaki et al. 2003; Kroemer et al. 2005), whereas slow release of cathepsins more likely operates through signaling pathways to trigger apoptosis (Kroemer et al. 2005). PubMed:22908190

Appears in Networks:

g(HBP:"APOE e4") increases bp(GO:"apoptotic process") View Subject | View Object

ApoE epsilon4 that trafficks to lysosomes more readily than ApoE epsilon3, promotes leakage of acid hydrolases, and induces apoptosis in cultured neuronal cells by forming membrane-damaging intermediates in the low-pHenvironment (Ji et al. 2002). PubMed:22908190

Appears in Networks:

composite(a(CHEBI:lactacystin), a(CHEBI:sirolimus)) decreases bp(GO:"apoptotic process") View Subject | View Object

Similar results have recently been observed in vitro using the proteasome inhibitor lactacystin, as pre-treatment with rapamycin attenuates lactacystin-induced apoptosis and reduces lactacystin-induced ubiquitinated protein aggregation [74]. PubMed:18930136

Appears in Networks:

bp(GO:"response to endoplasmic reticulum stress") increases bp(GO:"apoptotic process") 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:

p(HBP:"Tau oligomers", var("p.Lys280del")) increases bp(GO:"apoptotic process") 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

a(MESH:"RNA, Long Noncoding") increases bp(GO:"apoptotic process") View Subject | View Object

lncRNAs have been reported to cause apoptosis in the brain PubMed:30663117

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Alzheimer Disease

p(HGNC:PARK7) decreases bp(GO:"apoptotic process") View Subject | View Object

It also inhibits apoptosis and prevents the death of neuron PubMed:30663117

Appears in Networks:
Annotations
MeSH
Parkinson Disease

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

Amyloid-β has also been demonstrated to induce apoptosis via the JNK1/c-Jun/Fas ligand signaling cascade [110], which results in NF-κB activation PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

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

Recent evidence has cogently shown that Amyloid-β induces apoptosis in rat primary neurons and human post-mitotic neuronal cells by reducing Bcl-XL expression level and evoking the release of cytochrome c from the mitochondria in a NF-κB – dependent manner PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:etoposide) increases bp(GO:"apoptotic process") View Subject | View Object

Overexpression of the p65 subunit of NF-κB confers resistance to etoposide-induced apoptosis in cortical neurons PubMed:28745240

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Neurons
MeSH
Alzheimer Disease

bp(GO:"Fas signaling pathway") increases bp(GO:"apoptotic process") View Subject | View Object

Amyloid-β has also been demonstrated to induce apoptosis via the JNK1/c-Jun/Fas ligand signaling cascade [110], which results in NF-κB activation PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

bp(GO:"JNK cascade") increases bp(GO:"apoptotic process") View Subject | View Object

Amyloid-β has also been demonstrated to induce apoptosis via the JNK1/c-Jun/Fas ligand signaling cascade [110], which results in NF-κB activation PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

bp(MESH:"Oxidative Stress") increases bp(GO:"apoptotic process") View Subject | View Object

NF-κB activation also protects hippocampal neurons from oxidative stress-induced apoptosis by inducing manganese superoxide dismutase (MnSOD) expression and mitigating peroxynitrite-induced protein nitration PubMed:28745240

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

complex(GO:"NF-kappaB complex") decreases bp(GO:"apoptotic process") View Subject | View Object

Preponderance of evidence has implicated NF-κB as a survival factor in neurons [24, 114, 115] primarily because of the ability of NF-κB to suppress apoptosis in response to excitotoxic and apoptotic stimuli PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(GO:"NF-kappaB complex") decreases bp(GO:"apoptotic process") View Subject | View Object

The anti-apoptotic effects of NF-κB have been ascribed to its ability to trans-activate the expression of a multitude of anti-apoptotic genes such as Bcl-2, Bcl-XL, and Bfl-1/A1 in the neurons of the amygdala, olfactory bulb, and the CA1/CA3 region of the hippocampus PubMed:28745240

Appears in Networks:
Annotations
MeSH
Amygdala
MeSH
CA1 Region, Hippocampal
MeSH
CA3 Region, Hippocampal
MeSH
Olfactory Bulb
MeSH
Alzheimer Disease

p(HGNC:RELA) negativeCorrelation bp(GO:"apoptotic process") View Subject | View Object

Overexpression of the p65 subunit of NF-κB confers resistance to etoposide-induced apoptosis in cortical neurons PubMed:28745240

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Neurons
MeSH
Alzheimer Disease

p(HGNC:BCL2) decreases bp(GO:"apoptotic process") View Subject | View Object

The anti-apoptotic effects of NF-κB have been ascribed to its ability to trans-activate the expression of a multitude of anti-apoptotic genes such as Bcl-2, Bcl-XL, and Bfl-1/A1 in the neurons of the amygdala, olfactory bulb, and the CA1/CA3 region of the hippocampus PubMed:28745240

Appears in Networks:
Annotations
MeSH
Amygdala
MeSH
CA1 Region, Hippocampal
MeSH
CA3 Region, Hippocampal
MeSH
Olfactory Bulb
MeSH
Alzheimer Disease

p(HGNC:BCL2A1) decreases bp(GO:"apoptotic process") View Subject | View Object

The anti-apoptotic effects of NF-κB have been ascribed to its ability to trans-activate the expression of a multitude of anti-apoptotic genes such as Bcl-2, Bcl-XL, and Bfl-1/A1 in the neurons of the amygdala, olfactory bulb, and the CA1/CA3 region of the hippocampus PubMed:28745240

Appears in Networks:
Annotations
MeSH
Amygdala
MeSH
CA1 Region, Hippocampal
MeSH
CA3 Region, Hippocampal
MeSH
Olfactory Bulb
MeSH
Alzheimer Disease

p(HGNC:BCL2L1) decreases bp(GO:"apoptotic process") View Subject | View Object

The anti-apoptotic effects of NF-κB have been ascribed to its ability to trans-activate the expression of a multitude of anti-apoptotic genes such as Bcl-2, Bcl-XL, and Bfl-1/A1 in the neurons of the amygdala, olfactory bulb, and the CA1/CA3 region of the hippocampus PubMed:28745240

Appears in Networks:
Annotations
MeSH
Amygdala
MeSH
CA1 Region, Hippocampal
MeSH
CA3 Region, Hippocampal
MeSH
Olfactory Bulb
MeSH
Alzheimer Disease

p(HGNC:SOD2) decreases bp(GO:"apoptotic process") View Subject | View Object

Furthermore, Amyloid-β –induced NF-κB also results in the up-regulation of the antioxidant mitochondrial membrane enzyme – MnSOD (superoxide dismutase 2) [328] which is well known to combat oxidative stress and apoptosis PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(PUBCHEM:164676) decreases bp(GO:"apoptotic process") View Subject | View Object

Moreover, tanshinone IIA inhibited apoptosis in A 25-35-induced cells [232] and exerted anti-inflammatory activity in atherosclerosis and neuroprotective activity in cerebral ischemia/reperfusion impairment [233,234] PubMed:29179999

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Annotations
MeSH
Alzheimer Disease

a(CHEBI:nicorandil) decreases bp(GO:"apoptotic process") View Subject | View Object

Nicorandil, ATP-sensitive potassium channel opener, reduced apo- ptosis and decreased oxidative stress, downregulated APP695 mRNA and APP695 protein expression, also reduced Aβ 42 levels in the medium [90]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

p(FPLX:NFkappaB) association bp(GO:"apoptotic process") View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

act(p(HGNC:RELA)) increases bp(GO:"apoptotic process") View Subject | View Object

Further investigations confirm that the activation of p50 and RelA subunit contributes to the apoptotic program in cells exposed to the Aβ [17]. PubMed:27288790

Appears in Networks:

act(p(HGNC:NFKB1)) increases bp(GO:"apoptotic process") View Subject | View Object

Further investigations confirm that the activation of p50 and RelA subunit contributes to the apoptotic program in cells exposed to the Aβ [17]. PubMed:27288790

Appears in Networks:

bp(MESH:"Oxidative Stress") increases bp(GO:"apoptotic process") View Subject | View Object

In primary neuronal cells, exposure to Aβ25-35 peptide increase NF-κB mediated transactivation of manganese superoxide dismutase (Mn-SOD), suppress peroxinitrite production and inhibit membrane depolarization, thereby preventing apoptosis induced by oxidative stress PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neurons
MeSH
Alzheimer Disease

act(complex(GO:"NF-kappaB complex")) decreases bp(GO:"apoptotic process") View Subject | View Object

Complete abrogation of the DNA binding ability of NFκB factors induces apoptosis of the neuronal cells PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neurons

act(complex(GO:"NF-kappaB complex")) decreases bp(GO:"apoptotic process") View Subject | View Object

In primary neuronal cells, exposure to Aβ25-35 peptide increase NF-κB mediated transactivation of manganese superoxide dismutase (Mn-SOD), suppress peroxinitrite production and inhibit membrane depolarization, thereby preventing apoptosis induced by oxidative stress PubMed:25652642

Appears in Networks:
Annotations
MeSH
Neurons
MeSH
Alzheimer Disease

act(complex(p(HGNC:NFKB1), p(HGNC:RELA))) increases bp(GO:"apoptotic process") View Subject | View Object

Glutamate induced stimulation of cerebellar granule cells via the N-methyl-D-aspartate (NMDA) receptor activate p65:p50 dimers and enhance transactivation of pro-apoptotic factors PubMed:25652642

Appears in Networks:

path(MESH:"Porphyria, Erythropoietic") negativeCorrelation bp(GO:"apoptotic process") View Subject | View Object

However, in contrast to the bone marrow, there was no significant decrease between intermediate and late erythroblasts (Figure 2C) and we observed decreased rather than increased apoptosis, as usually observed in ineffective erythropoiesis22,23 (Figure 2D). PubMed:28143953

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Spleen
MeSH
Porphyria, Erythropoietic
Text Location
Results

Out-Edges 13

bp(GO:"apoptotic process") association p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits") View Subject | View Object

Thus, it seems that nAChRs may play a role in mediating Abeta toxicity through synergistic mechanisms; in addition to possible direct interactions (binding), nAChRs may also result in accelerated cell death through enhancing intracellular Abeta accumulation. PubMed:19293145

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bp(GO:"apoptotic process") association p(HGNC:MAPT, frag("?", "17kD")) 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

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Experimental Factor Ontology (EFO)
PC12
Text Location
Review

bp(GO:"apoptotic process") increases act(p(HGNC:CASP6)) View Subject | View Object

There may be reciprocity with the apoptosis pathway as activating caspase-3 by inducing apoptosis in cortical neuronal culture led to tau cleavage (22), and selectively expressing tauC3 led to apoptosis in NT2 and COS cells (21). This might represent a feed-forward loop of neurotoxicity. PubMed:24027553

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Text Location
Review

bp(GO:"apoptotic process") association r(HGNC:GAPDH) View Subject | View Object

A relationship has recently been reported between the expression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and apoptotic events14. Real-time RT-PCR experiments showed that the expression of GAPDH was significantly increased by the addition of GA (Fig. 2a). These results suggested that GA caused cell toxicity concomitant with increases in the gene expression of GAPDH in SH-SY5Y cells. PubMed:26304819

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bp(GO:"apoptotic process") negativeCorrelation p(HGNC:MAPT, pmod(Ph, Ser, 262)) View Subject | View Object

These data suggest that tau hyperphosphorylation at Thr231, Ser262, and Ser396 by DAPK1 renders the cells more resistant to the kinase-induced apoptotic cell death, providing new insights into the tau-involved apoptotic abortion in the course of chronic neurodegeneration. PubMed:23948915

Appears in Networks:

bp(GO:"apoptotic process") negativeCorrelation p(HGNC:MAPT, pmod(Ph, Ser, 396)) View Subject | View Object

These data suggest that tau hyperphosphorylation at Thr231, Ser262, and Ser396 by DAPK1 renders the cells more resistant to the kinase-induced apoptotic cell death, providing new insights into the tau-involved apoptotic abortion in the course of chronic neurodegeneration. PubMed:23948915

Appears in Networks:

bp(GO:"apoptotic process") negativeCorrelation p(HGNC:MAPT, pmod(Ph, Thr, 231)) View Subject | View Object

These data suggest that tau hyperphosphorylation at Thr231, Ser262, and Ser396 by DAPK1 renders the cells more resistant to the kinase-induced apoptotic cell death, providing new insights into the tau-involved apoptotic abortion in the course of chronic neurodegeneration. PubMed:23948915

Appears in Networks:

bp(GO:"apoptotic process") positiveCorrelation act(p(HGNC:GSK3B)) View Subject | View Object

Apart from affecting tau phosphorylation, abnormal activation of GSK3β, cdk5, and ERK has been linked to cytoskeletal abnormalities (microtubules, neurofilaments), alterations in amyloid precursor protein (APP) phosphorylation and processing, impairment of neurogenesis, alterations in synaptic plasticity and induction of apoptotic processes (Reviewed in Crews and Masliah, 2010; Medina and Avila, 2013, 2014). PubMed:24653673

Appears in Networks:

bp(GO:"apoptotic process") positiveCorrelation act(p(HGNC:CDK5)) View Subject | View Object

Apart from affecting tau phosphorylation, abnormal activation of GSK3β, cdk5, and ERK has been linked to cytoskeletal abnormalities (microtubules, neurofilaments), alterations in amyloid precursor protein (APP) phosphorylation and processing, impairment of neurogenesis, alterations in synaptic plasticity and induction of apoptotic processes (Reviewed in Crews and Masliah, 2010; Medina and Avila, 2013, 2014). PubMed:24653673

Appears in Networks:

bp(GO:"apoptotic process") positiveCorrelation act(p(FPLX:ERK)) View Subject | View Object

Apart from affecting tau phosphorylation, abnormal activation of GSK3β, cdk5, and ERK has been linked to cytoskeletal abnormalities (microtubules, neurofilaments), alterations in amyloid precursor protein (APP) phosphorylation and processing, impairment of neurogenesis, alterations in synaptic plasticity and induction of apoptotic processes (Reviewed in Crews and Masliah, 2010; Medina and Avila, 2013, 2014). PubMed:24653673

Appears in Networks:

bp(GO:"apoptotic process") negativeCorrelation p(HGNC:RELA) View Subject | View Object

Overexpression of the p65 subunit of NF-κB confers resistance to etoposide-induced apoptosis in cortical neurons PubMed:28745240

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Neurons
MeSH
Alzheimer Disease

bp(GO:"apoptotic process") association p(FPLX:NFkappaB) View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

bp(GO:"apoptotic process") negativeCorrelation path(MESH:"Porphyria, Erythropoietic") View Subject | View Object

However, in contrast to the bone marrow, there was no significant decrease between intermediate and late erythroblasts (Figure 2C) and we observed decreased rather than increased apoptosis, as usually observed in ineffective erythropoiesis22,23 (Figure 2D). PubMed:28143953

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Spleen
MeSH
Porphyria, Erythropoietic
Text Location
Results

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.