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p(HGNC:IL18)

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Entity

Name
IL18
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 5

Inflammasome activation and innate immunity in Alzheimer’s disease v1.0.2

Activation and regulation of the inflammasomes v1.0.0

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

Inflammasome Involvement in Alzheimer’s Disease v1.0.0

Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0

In-Edges 38

complex(GO:"inflammasome complex") increases p(HGNC:IL18) View Subject | View Object

IL-1β and IL-18 are synthesized as inactive precursors, proIL-1β and proIL-18, respectively, and require inflammasomes for their maturation PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

act(complex(GO:"NLRP3 inflammasome complex")) increases p(HGNC:IL18) View Subject | View Object

Activation of NLRP3 leads to the generation of interleukin-1b (IL-1b) and interleukin 18 (IL-18), which are being cleaved by caspase-1 from their inactive precursors and subsequently PubMed:28019679

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:CASP1) increases act(p(HGNC:IL18)) View Subject | View Object

Activation of NLRP3 leads to the generation of interleukin-1b (IL-1b) and interleukin 18 (IL-18), which are being cleaved by caspase-1 from their inactive precursors and subsequently PubMed:28019679

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

a(MESH:"Interferon Type I") decreases sec(p(HGNC:IL18)) View Subject | View Object

In addition, type I IFNs can reduce IL-1β and IL-18 release by functioning at two levels. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Interferon signaling subgraph
NeuroMMSigDB
Interleukin signaling subgraph

bp(GO:"cell activation") increases p(HGNC:IL18) View Subject | View Object

The transcription of pro-IL-1β is induced by the activation of the transcription factor nuclear factor-κB (NF-κB), whereas pro-IL-18 is constitutively expressed and its expression is increased after cellular activation. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph
NeuroMMSigDB
Nuclear factor Kappa beta subgraph

complex(GO:"inflammasome complex") increases act(p(HGNC:IL18)) View Subject | View Object

Inflammasomes are key signalling platforms that detect pathogenic microorganisms and sterile stressors, and that activate the highly pro-inflammatory cytokines interleukin-1β (IL-1β) and IL-18. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL18)) View Subject | View Object

Once the protein complexes have formed, the inflammasomes activate caspase 1, which proteolytically activates the pro-inflammatory cytokines interleukin-1β (IL-1β)3 and IL-18. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL18)) View Subject | View Object

Active caspase 1 proteolytically activates a number of proteins8, including pro-IL-1β and pro-IL-18 (REFS 9,10), and induces their release via a non-classical secretion pathway11. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases sec(p(HGNC:IL18)) View Subject | View Object

Active caspase 1 proteolytically activates a number of proteins8, including pro-IL-1β and pro-IL-18 (REFS 9,10), and induces their release via a non-classical secretion pathway11. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP8)) regulates act(p(HGNC:IL18)) View Subject | View Object

In addition, it was recently shown that CD95 signalling mediates IL-1β and IL-18 processing through the activation of caspase 8 (REF. 60) (FIG. 1). PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph
NeuroMMSigDB
Tumor necrosis factor subgraph

a(CHEBI:probenecid) decreases p(HGNC:IL18) View Subject | View Object

Probenecid, an inhibitor of pannexin 1, has been shown to significantly inhibit the expression and activation of the NLRP2 inflammasome, and the maturation of bothIL-1β and IL-18 in human astrocytes induced by ATP (Minkiewicz et al., 2013) PubMed:24561250

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

bp(GO:aging) increases p(HGNC:IL18) View Subject | View Object

Aging, another risk factor of AD, has been found to activate the NLRP1 inflammasome and upregulate IL-18 and IL-1β levels in the hippocampus of aged mice (Mawhinney et al., 2011) PubMed:24561250

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Hippocampus
NeuroMMSigDB
Interleukin signaling subgraph

act(complex(GO:"NLRP1 inflammasome complex")) increases sec(p(HGNC:IL18)) View Subject | View Object

Spinal cord injury causes IL-18 and IL-1β release from neuronal cells through the activation of the NLRP1 inflammasome, composed of receptor NLRP1, adaptor protein ASC, caspase-1, caspase-11 and X-linked inhibitor of apoptosis protein (de Rivero Vaccari et al., 2008) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons
NeuroMMSigDB
Interleukin signaling subgraph

complex(GO:"inflammasome complex") positiveCorrelation p(HGNC:IL18) View Subject | View Object

Inflammasomes involve in the maturation of IL-1β and IL-18 are expressed in neurons (de Rivero Vaccari et al., 2008; Yang-Wei Fann et al., 2013; Zou and Crews, 2012) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons
NeuroMMSigDB
Interleukin signaling subgraph

act(complex(GO:"inflammasome complex")) increases p(HGNC:IL18) View Subject | View Object

Like IL-1β, in most cases, the mature secretable form of IL-18 is generated by caspase-1 through the activation of inflammasome PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

complex(GO:"inflammasome complex") regulates p(HGNC:IL18) View Subject | View Object

However the maturation of IL-18 and IL-1β could be regulated by the same type of inflammasome PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:CASP1) increases p(HGNC:IL18) View Subject | View Object

Caspase-1 is the protease that cleaves the precursor of the proinflammatory molecules to form their mature form, such as IL-1β and IL-18 (Schroder and Tschopp, 2010) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:CASP1) increases p(HGNC:IL18) View Subject | View Object

Like IL-1β, in most cases, the mature secretable form of IL-18 is generated by caspase-1 through the activation of inflammasome PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:NLRP1) increases p(HGNC:IL18) View Subject | View Object

For example, down-regulation of NLRP1 in macrophages trigger by Cordyceps sinensis mycelium reduces both IL-18 and IL-1β levels (Huang et al., 2013) PubMed:24561250

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:PYCARD) increases p(HGNC:IL18) View Subject | View Object

ASC neutralization reduces the upregulation in IL-18 and IL-1β levels (de Rivero Vaccari et al., 2008) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

composite(complex(GO:"inflammasome complex"), p(HGNC:NLRP2)) increases p(HGNC:IL18) 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

p(HGNC:PANX1) increases p(HGNC:IL18) View Subject | View Object

Probenecid, an inhibitor of pannexin 1, has been shown to significantly inhibit the expression and activation of the NLRP2 inflammasome, and the maturation of bothIL-1β and IL-18 in human astrocytes induced by ATP (Minkiewicz et al., 2013) PubMed:24561250

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

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:IL18) View Subject | View Object

Interleukins, in particular IL-1β and IL-18, are upregulated in AD brain, and the overexpression of IL-1β or IL-18 is critical for the onset of the inflammatory process (Rubio-Perez and Morillas-Ruiz, 2012), and both mediate the expression of a vast array of inflammatory genes (Weber et al., 2010) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Inflammatory response subgraph
NeuroMMSigDB
Interleukin signaling subgraph

path(MESH:"Spinal Cord Injuries") increases sec(p(HGNC:IL18)) View Subject | View Object

Spinal cord injury causes IL-18 and IL-1β release from neuronal cells through the activation of the NLRP1 inflammasome, composed of receptor NLRP1, adaptor protein ASC, caspase-1, caspase-11 and X-linked inhibitor of apoptosis protein (de Rivero Vaccari et al., 2008) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons
NeuroMMSigDB
Interleukin signaling subgraph

bp(GO:"astrocyte activation") increases sec(p(HGNC:IL18)) View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Brain
MeSH
Cerebrospinal Fluid
MeSH
Serum
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph
NeuroMMSigDB
Nitric oxide subgraph

bp(GO:"microglial cell activation") increases sec(p(HGNC:IL18)) View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Brain
MeSH
Cerebrospinal Fluid
MeSH
Serum
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph
NeuroMMSigDB
Nitric oxide subgraph

complex(GO:"inflammasome complex") increases act(p(HGNC:IL18)) View Subject | View Object

Inflammasomes are responsible for the maturation of pro-inflammatory cytokines such as interleukin (IL)-1beta, IL-18, and IL-33 and activation of inflammatory cell death, pyroptosis. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL18)) View Subject | View Object

Post activation of the inflammasome, caspase 1 enzyme initiates the maturation of pro-inflammatory cytokines particularly interleukin (IL)-1beta, IL-18, and IL-33 [4] (Fig. 1),and inflammation mediated cell death occurs via the nucleotide-binding domain and leucine-rich repeat(NLR) family of proteins [5]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

sec(p(HGNC:CASP1)) increases act(p(HGNC:IL18)) View Subject | View Object

In AD, microglial cells and astrocytes express NLRP3, which in turn can detect A beta plaques and act by secreting caspase-1 to activate IL-1 beta and IL- 18 [23–25]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL18)) View Subject | View Object

Both IL-1 beta and IL-18 are generated in their mature secreted form by caspase-1 through activa- tion of the inflammasome. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CASP1)) increases act(p(HGNC:IL18)) View Subject | View Object

Once activated, caspase-1 promotes the maturation of the proin- flammatory cytokines IL-1 beta , IL-18, and IL-33. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(FPLX:ELA)) increases p(HGNC:IL18) View Subject | View Object

However, IL- 18 can be derived as a byproduct from the activities of various extracellular enzymes such as protease 3, serine protease, elastase and cathepsin G [62–65]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:CTSG)) increases p(HGNC:IL18) View Subject | View Object

However, IL- 18 can be derived as a byproduct from the activities of various extracellular enzymes such as protease 3, serine protease, elastase and cathepsin G [62–65]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:PRSS3)) increases p(HGNC:IL18) View Subject | View Object

However, IL- 18 can be derived as a byproduct from the activities of various extracellular enzymes such as protease 3, serine protease, elastase and cathepsin G [62–65]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:IL18) View Subject | View Object

Increased levels of IL-1 beta and IL-18 have been detected in serum, cerebrospinal fluid, and brains of patients with AD and in other forms of dementia [42–46]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Cerebrospinal Fluid
MeSH
Serum
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph

path(MESH:"Alzheimer Disease") association p(HGNC:IL18) View Subject | View Object

Both these studies indicated an important role of IL-18 in AD. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph

path(MESH:Dementia) positiveCorrelation p(HGNC:IL18) View Subject | View Object

Increased levels of IL-1 beta and IL-18 have been detected in serum, cerebrospinal fluid, and brains of patients with AD and in other forms of dementia [42–46]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Cerebrospinal Fluid
MeSH
Serum
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:IL18) View Subject | View Object

TNF-α [27], IL-1β [28], IL-18 [29], CXCL10 [30] and TGF-β1 [31] are known to be elevated in the AD brain. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Brain

Out-Edges 13

p(HGNC:IL18) positiveCorrelation complex(GO:"inflammasome complex") View Subject | View Object

Inflammasomes involve in the maturation of IL-1β and IL-18 are expressed in neurons (de Rivero Vaccari et al., 2008; Yang-Wei Fann et al., 2013; Zou and Crews, 2012) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:IL18) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Interleukins, in particular IL-1β and IL-18, are upregulated in AD brain, and the overexpression of IL-1β or IL-18 is critical for the onset of the inflammatory process (Rubio-Perez and Morillas-Ruiz, 2012), and both mediate the expression of a vast array of inflammatory genes (Weber et al., 2010) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Inflammatory response subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:IL18) increases bp(GO:"inflammatory response") View Subject | View Object

Interleukins, in particular IL-1β and IL-18, are upregulated in AD brain, and the overexpression of IL-1β or IL-18 is critical for the onset of the inflammatory process (Rubio-Perez and Morillas-Ruiz, 2012), and both mediate the expression of a vast array of inflammatory genes (Weber et al., 2010) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Inflammatory response subgraph
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:IL18) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Increased levels of IL-1 beta and IL-18 have been detected in serum, cerebrospinal fluid, and brains of patients with AD and in other forms of dementia [42–46]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Cerebrospinal Fluid
MeSH
Serum
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:IL18) association path(MESH:"Alzheimer Disease") View Subject | View Object

Both these studies indicated an important role of IL-18 in AD. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:IL18) positiveCorrelation path(MESH:Dementia) View Subject | View Object

Increased levels of IL-1 beta and IL-18 have been detected in serum, cerebrospinal fluid, and brains of patients with AD and in other forms of dementia [42–46]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Cerebrospinal Fluid
MeSH
Serum
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:IL18) increases bp(GO:"microglial cell activation") View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Brain
MeSH
Cerebrospinal Fluid
MeSH
Serum
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph
NeuroMMSigDB
Nitric oxide subgraph

p(HGNC:IL18) increases bp(GO:"astrocyte activation") View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
Medium
MeSH
Brain
MeSH
Cerebrospinal Fluid
MeSH
Serum
MeSH
Alzheimer Disease
NeuroMMSigDB
Interleukin signaling subgraph
NeuroMMSigDB
Nitric oxide subgraph

p(HGNC:IL18) increases a(CHEBI:"amyloid-beta") View Subject | View Object

Pro-inflammatory IL-18 increases AD-associated A beta deposition in human neuron-like cells in culture [55]. IL-18 also increases the expression of glycogen synthase kinase 3 beta (GSK-3 beta ) and cyclin-dependent kinase 5, both of which are involved in hyperphos- phorylation of the tau protein [56]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Cyclin-CDK subgraph
NeuroMMSigDB
GSK3 subgraph
NeuroMMSigDB
Interleukin signaling subgraph
NeuroMMSigDB
Tau protein subgraph

p(HGNC:IL18) increases p(HGNC:GSK3B) View Subject | View Object

Pro-inflammatory IL-18 increases AD-associated A beta deposition in human neuron-like cells in culture [55]. IL-18 also increases the expression of glycogen synthase kinase 3 beta (GSK-3 beta ) and cyclin-dependent kinase 5, both of which are involved in hyperphos- phorylation of the tau protein [56]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Cyclin-CDK subgraph
NeuroMMSigDB
GSK3 subgraph
NeuroMMSigDB
Interleukin signaling subgraph
NeuroMMSigDB
Tau protein subgraph

p(HGNC:IL18) increases p(HGNC:CDK5) View Subject | View Object

Pro-inflammatory IL-18 increases AD-associated A beta deposition in human neuron-like cells in culture [55]. IL-18 also increases the expression of glycogen synthase kinase 3 beta (GSK-3 beta ) and cyclin-dependent kinase 5, both of which are involved in hyperphos- phorylation of the tau protein [56]. PubMed:27314526

Appears in Networks:
Annotations
Confidence
High
MeSH
Alzheimer Disease
NeuroMMSigDB
Amyloidogenic subgraph
NeuroMMSigDB
Cyclin-CDK subgraph
NeuroMMSigDB
GSK3 subgraph
NeuroMMSigDB
Interleukin signaling subgraph
NeuroMMSigDB
Tau protein subgraph

p(HGNC:IL18) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

TNF-α [27], IL-1β [28], IL-18 [29], CXCL10 [30] and TGF-β1 [31] are known to be elevated in the AD brain. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Brain

p(HGNC:IL18) increases act(p(FPLX:NFkappaB)) View Subject | View Object

Cortical neurons stimulated with IL-18 also generated NF-κB activation [33]. PubMed:27288790

Appears in Networks:
Annotations
Cell Ontology (CL)
cerebral cortex neuron

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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.