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p(HGNC:IL1B)

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Entity

Name
IL1B
Namespace
hgnc
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/hgnc-symbols.belns

Appears in Networks 12

Nuclear receptors as therapeutic targets for Alzheimer's disease. v1.0.0

Anti-inflammatory activity of anatabine via inhibition of STAT3 phosphorylation v1.0.0

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

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

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

Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0

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 88

a(HBP:HBP00089) increases sec(p(HGNC:IL1B)) View Subject | View Object

The plaque-associated microglia secrete a variety of cytotoxic species including the inflammatory cytokines, INF-g, TNF-a, IL-1b and IL-6 and chemokines, most prominently CCL2 [10-12]. PubMed:21718217

Appears in Networks:
Annotations
Confidence
High
MeSH
Microglia

a(CHEBI:lipopolysaccharide) increases p(HGNC:IL1B) View Subject | View Object

Anatabine at 200 mg/ ml significantly lowered LPS induced IL-1b levels in whole blood (Mann–Whitney U=0.0, Z=-2.3, P=0.02) PubMed:23178521

Appears in Networks:

composite(a(CHEBI:Anatabine), a(CHEBI:lipopolysaccharide), a(MESH:Blood)) decreases p(HGNC:IL1B) View Subject | View Object

Higher doses of anatabine resulted in a complete suppression of IL-1b levels in LPS challenged human blood (Mann–Whitney U=0.0, Z=-2.5, P=0.01) PubMed:23178521

Appears in Networks:

composite(a(CHEBI:Anatabine), a(MESH:Blood)) decreases p(HGNC:IL1B) View Subject | View Object

Anatabine at 200 mg/ ml significantly lowered LPS induced IL-1b levels in whole blood (Mann–Whitney U=0.0, Z=-2.3, P=0.02) PubMed:23178521

Appears in Networks:

a(GO:"neurofibrillary tangle") increases p(HGNC:IL1B) 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

act(complex(GO:"NLRP3 inflammasome complex")) increases p(HGNC:IL1B) 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(CHEBI:paraquat) increases p(HGNC:IL1B) View Subject | View Object

Using the herbizide, N,N0-dimethyl-4,40-bipyridinium dichloride (paraquat) as a mitochondrial toxin, which is known to induce oxidative stress, Chen et al. found increased levels of caspase-1 and IL-1b in brain of wild type and APP/PS1 transgenic mice (2), suggesting that those were due to NLRP3 inflammasome activation PubMed:28019679

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

act(complex(GO:"NLRP3 inflammasome complex")) increases p(HGNC:IL1B) View Subject | View Object

Using the herbizide, N,N0-dimethyl-4,40-bipyridinium dichloride (paraquat) as a mitochondrial toxin, which is known to induce oxidative stress, Chen et al. found increased levels of caspase-1 and IL-1b in brain of wild type and APP/PS1 transgenic mice (2), suggesting that those were due to NLRP3 inflammasome activation PubMed:28019679

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

p(HGNC:CASP1) increases act(p(HGNC:IL1B)) 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(CHEBI:"potassium(1+)") decreases sec(p(HGNC:IL1B)) View Subject | View Object

In addition, high extracellular levels of K+ can block IL-1β release after NLRC4 and AIM2 inflammasome formation80,81, which indicates that low intracellular K+ levels might also be required for the activation of these inflammasomes. PubMed:23702978

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

a(MESH:"Interferon Type I") decreases sec(p(HGNC:IL1B)) 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

a(MESH:Interferons) decreases p(HGNC:IL1B) View Subject | View Object

IFNs upregulate AIM2 expression but they downregulate IL-1β expression and inhibit the NLRP3 inflammasome. PubMed:23702978

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

bp(GO:autophagy) decreases sec(p(HGNC:IL1B)) View Subject | View Object

For inflammasome activation and IL-1β release, autophagy is a negative regulator: PubMed:23702978

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

complex(GO:"inflammasome complex") increases act(p(HGNC:IL1B)) 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:IL1B)) 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:IL1B)) 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:IL1B)) 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 act(p(HGNC:IL1B)) View Subject | View Object

Caspase 1mediated activation of members of the IL-1β cytokine family leads to the recruitment and the activation of other immune cells, such as neutrophils, at the site of infection and/or tissue damage. PubMed:23702978

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

p(HGNC:CASP8) increases act(p(HGNC:IL1B)) View Subject | View Object

One additional factor that can mediate IL-1β processing and activation is caspase 8 (FIG. 1) PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph

act(p(HGNC:CASP8)) increases act(p(HGNC:IL1B)) View Subject | View Object

In the presence of the translation inhibitor cycloheximide, TRIF signalling that is downstream of TLR3 or TLR4 leads to pro-IL-1β processing by caspase 8 (REF. 55). PubMed:23702978

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

act(p(HGNC:CASP8)) regulates act(p(HGNC:IL1B)) 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

complex(p(HGNC:CASP8), p(HGNC:MALT1), p(HGNC:PYCARD)) increases act(p(HGNC:IL1B)) View Subject | View Object

For example, following sensing of fungal components by the PRR dectin 1 that is expressed on human dendritic cells, signalling via the kinase SYK leads to the formation of a complex that is composed of caspase 8 and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1); this complex binds to ASC, which possibly recruits cleavage substrates53. The MALT1-ASC-caspase 8 complex directly mediates IL-1β maturation53. PubMed:23702978

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

act(p(FPLX:TLR)) increases p(HGNC:IL1B) View Subject | View Object

First, a bacterial Toll-like receptor (TLR) activator leads to cellular priming and upregulation of NLRP3 and pro-IL-1β expression (the priming checkpoint in the standard model)37,38. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:CARD17) decreases p(HGNC:IL1B) View Subject | View Object

CARD17 (also known as INCA), which is another decoy protein, is upregulated by IFNγ to suppress IL-1β generation114. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
MeSH
Extracellular Space
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interferon signaling subgraph
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:FAS)) increases act(p(HGNC:IL1B)) View Subject | View Object

Indeed, activation of the TNFR family member CD95 (also known as FAS) can induce IL-1β processing that is independent of inflammasomes and of caspase 1 (REF. 59). PubMed:23702978

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

p(HGNC:NFKB1) increases p(HGNC:IL1B) 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

p(HGNC:PRTN3) increases act(p(HGNC:IL1B)) View Subject | View Object

Indeed, a number of non-caspase proteases such as proteinase 3 have the ability to activate IL-1β in an inflammasome-independent manner11. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

act(p(HGNC:RIPK3)) increases act(p(HGNC:IL1B)) View Subject | View Object

The formation of this complex activates RIP3, which is necessary for the cleavage of pro-IL-1β by both the NLRP3-caspase 1 and the caspase 8 pathways56 (FIG. 1). PubMed:23702978

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

a(CHEBI:"saturated fatty acid") increases p(HGNC:IL1B) View Subject | View Object

These studies highlighted the role of saturated fatty acids in the production of IL-1β by inflammasomes, i.e. NLRC4 PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

a(CHEBI:probenecid) decreases p(HGNC:IL1B) 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:IL1B) 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

complex(GO:"IPAF inflammasome complex") increases p(HGNC:IL1B) View Subject | View Object

In the CNS, the production of IL-1β by inflammasomes, specifically NLRP1, NLRP2, NLRP3 and NLRC4, is well-characterized as compared to other interleukins (Minkiewicz et al., 2013; Trendelenburg, 2008) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Central Nervous System
NeuroMMSigDB
Interleukin signaling subgraph

complex(GO:"IPAF inflammasome complex") increases sec(p(HGNC:IL1B)) View Subject | View Object

Palmitate, a fatty acid, activates the NLRC4 inflammasome in primary astrocytes leading to the release of IL-1β (Liu and Chan, 2014) PubMed:24561250

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

act(complex(GO:"IPAF inflammasome complex")) increases sec(p(HGNC:IL1B)) View Subject | View Object

Recently we identify that palmitate activates the NLRC4 inflammasome in primary astrocytes to release IL-1β, and ASC participates in the activation of the NLRC4 inflammasome (Liu and Chan, 2014) PubMed:24561250

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

complex(GO:"IPAF inflammasome complex") increases p(HGNC:IL1B) View Subject | View Object

These studies highlighted the role of saturated fatty acids in the production of IL-1β by inflammasomes, i.e. NLRC4 PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

complex(GO:"NLRP1 inflammasome complex") increases p(HGNC:IL1B) View Subject | View Object

In the CNS, the production of IL-1β by inflammasomes, specifically NLRP1, NLRP2, NLRP3 and NLRC4, is well-characterized as compared to other interleukins (Minkiewicz et al., 2013; Trendelenburg, 2008) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Central Nervous System
NeuroMMSigDB
Interleukin signaling subgraph

act(complex(GO:"NLRP1 inflammasome complex")) increases p(HGNC:IL1B) View Subject | View Object

Spinal cord injury can activate the NLRP1 inflammasome to produce IL-1β in rat spinal cord neurons (de Rivero Vaccari et al., 2008) PubMed:24561250

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

act(complex(GO:"NLRP1 inflammasome complex")) increases sec(p(HGNC:IL1B)) 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:"NLRP3 inflammasome complex") increases p(HGNC:IL1B) View Subject | View Object

In the CNS, the production of IL-1β by inflammasomes, specifically NLRP1, NLRP2, NLRP3 and NLRC4, is well-characterized as compared to other interleukins (Minkiewicz et al., 2013; Trendelenburg, 2008) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Central Nervous System
NeuroMMSigDB
Interleukin signaling subgraph

complex(GO:"NLRP3 inflammasome complex") increases p(HGNC:IL1B) View Subject | View Object

In vivo and cell studies demonstrate that fibrillar Aβ activates the NLRP3 inflammasome which is composed of the NLRP3 receptor, ASC and caspase-1, to produce IL-1β in microglia (Halle et al., 2008) PubMed:24561250

Appears in Networks:
Annotations
Cell Ontology (CL)
microglial cell
Confidence
Medium
NeuroMMSigDB
Amyloidogenic subgraph

complex(GO:"inflammasome complex") positiveCorrelation p(HGNC:IL1B) 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

complex(GO:"inflammasome complex") increases p(HGNC:IL1B) 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

complex(GO:"inflammasome complex") regulates p(HGNC:IL1B) 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:IL1B) 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:NLRP1) increases p(HGNC:IL1B) 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:IL1B) 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(a(CHEBI:hexadecanoate), p(HGNC:NLRC4)) increases p(HGNC:IL1B) View Subject | View Object

Reducing NLRC4 or ASC levels in the palmitate (PA)-treated astrocytes significantly reduces IL-1β production (Liu and Chan, 2014) PubMed:24561250

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

composite(a(CHEBI:hexadecanoate), p(HGNC:PYCARD)) increases p(HGNC:IL1B) View Subject | View Object

Reducing NLRC4 or ASC levels in the palmitate (PA)-treated astrocytes significantly reduces IL-1β production (Liu and Chan, 2014) PubMed:24561250

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

composite(complex(GO:"inflammasome complex"), p(HGNC:NLRP2)) increases p(HGNC:IL1B) View Subject | View Object

In the CNS, the production of IL-1β by inflammasomes, specifically NLRP1, NLRP2, NLRP3 and NLRC4, is well-characterized as compared to other interleukins (Minkiewicz et al., 2013; Trendelenburg, 2008) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
MeSH
Central Nervous System
NeuroMMSigDB
Interleukin signaling subgraph

composite(complex(GO:"inflammasome complex"), p(HGNC:NLRP2)) increases p(HGNC:IL1B) 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

composite(complex(GO:"inflammasome complex"), p(HGNC:NLRP2), p(HGNC:P2RX7), p(HGNC:PANX1)) increases p(HGNC:IL1B) View Subject | View Object

The ATP-induced activation of the NLRP2 inflammasome interacts with the ATP-release pannexin 1 channel and ATP-gated P2X7 receptor leading to the maturation of IL-1β (Minkiewicz et al., 2013) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:PANX1) increases p(HGNC:IL1B) 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

p(MGI:P2rx4) increases p(HGNC:IL1B) View Subject | View Object

However, upon further study of purinergic receptor P2X4 knockout mice with spinal cord injury, the production of IL-1β but not of IL-18 reduces in the neurons as compared with wild-type mice (de Rivero Vaccari et al., 2012) PubMed:24561250

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

p(MGI:P2rx4) increases p(HGNC:IL1B) View Subject | View Object

P2X4 knock-out mice has been shown to decrease the level of IL-1β and to have impair inflammasome signaling (de Rivero Vaccari et al., 2012) PubMed:24561250

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:IL1B) 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:IL1B)) 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

a(MESH:Astrocytes) increases sec(p(HGNC:IL1B)) View Subject | View Object

NO can also bring about apoptosis of hippocampal neurons via caspase- 3 activity [50] whereas astrocyte-secreted IL-1 beta can increase the production of APP and A beta from neu- rons [51–53] (Fig. 1). PubMed:27314526

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

bp(GO:"astrocyte activation") increases sec(p(HGNC:IL1B)) 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:IL1B)) 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:IL1B)) 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:IL1B)) 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:IL1B)) 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:IL1B)) 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:IL1B)) 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

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:IL1B) 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:Dementia) positiveCorrelation p(HGNC:IL1B) 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

a(CHEBI:"alpha-tocopherol") decreases p(HGNC:IL1B) View Subject | View Object

Furthermore, it disrupted the activity of NF-B, and thus, caused the suppression of NO synthase and inflammatory regulators such as IL-6 and IL-1, and the reduction of microglial activation [37] PubMed:29179999

Appears in Networks:

act(a(MESH:Microglia)) increases p(HGNC:IL1B) View Subject | View Object

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(GO:"NF-kappaB complex") regulates p(HGNC:IL1B) View Subject | View Object

It is well established that NF-κB is one of the most prominent transcription factors that regulates IL1β production PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(GO:"NF-kappaB complex") increases p(HGNC:IL1B) View Subject | View Object

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"1,8-cineole") decreases p(HGNC:IL1B) View Subject | View Object

The expression of pro-inflammatory cytokines such as TNF-, IL-1 and IL-6 were significantly reduced by treatment of 1,8-cineole in A 25-35-induced cells [250]. PubMed:29179999

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"amyloid-beta") increases sec(p(HGNC:IL1B)) View Subject | View Object

Glial activation, pro-inflammatory gene expression and elevated secretion of IL-1, IL-6 and TNF- are consequences of high A levels [30,31]. PubMed:29179999

Appears in Networks:

a(CHEBI:Geniposide) decreases p(HGNC:IL1B) View Subject | View Object

Geniposide considerably suppressed RAGE-related signaling such as ERK and IB/NF-B, the expression of TNF-, IL-1 and cerebral A accumulation in vivo[245] PubMed:29179999

Appears in Networks:

a(PUBCHEM:102336202) decreases p(HGNC:IL1B) View Subject | View Object

Xanthoceraside decreased the expression of A 25-35/IFN--stimulated NO, IL-1,and TNF- in microglia, which implicated the down-regulation of the activities of MAPK and NF-B pathways [248] PubMed:29179999

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

a(PUBCHEM:442534) decreases p(HGNC:IL1B) View Subject | View Object

It attenuated the development of AD by inhibiting glycogen synthase kinase 3 (GSK-3) and NF-B activation, and sup-pressing the NLRP3 inflammasome and cytokines such as TNF-and IL-1 [1]. PubMed:29179999

Appears in Networks:

a(PUBCHEM:73078) decreases p(HGNC:IL1B) View Subject | View Object

It ameliorated spatial learning and memory disorder, which was caused by A 1-42 and was associated with the inter-ference of NF-B activity and the inhibition of IL-1 and TNF-expression [183]. PubMed:29179999

Appears in Networks:

a(MESH:Lipopolysaccharides) increases p(HGNC:IL1B) View Subject | View Object

LPS treatment induced the nuclear translocation of NF-κB and increased the expression and secretion of TNF-α and IL-1β [63]. PubMed:27288790

Appears in Networks:

a(MESH:Lipopolysaccharides) increases sec(p(HGNC:IL1B)) View Subject | View Object

LPS treatment induced the nuclear translocation of NF-κB and increased the expression and secretion of TNF-α and IL-1β [63]. PubMed:27288790

Appears in Networks:

act(p(FPLX:NFkappaB)) increases p(HGNC:IL1B) View Subject | View Object

Then the stimulation of RAGE is able to activate the mitogen-activated protein kinase signaling cascades which converge in IκB kinase complex to phosphorylate IκB, thereby release and activate NF-κB, thus trigger NF-κB dependent gene transcription including IL-1β and TNF-α, which in turn induce the translocation of NF-κB to the nucleus [50]. PubMed:27288790

Appears in Networks:

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:IL1B) 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

complex(GO:"NF-kappaB complex") increases p(HGNC:IL1B) View Subject | View Object

Increased presence of NF-κB mediated IL-1β, IL-6, and TNF-α cytokines have been reported in the affected tissues, serum and CSF of AD patients PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:IL1B) View Subject | View Object

Increased presence of NF-κB mediated IL-1β, IL-6, and TNF-α cytokines have been reported in the affected tissues, serum and CSF of AD patients PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:heme) increases p(HGNC:IL1B) View Subject | View Object

. Heme activates macrophages inducing the production of TNF, KC (Figueiredo et al., 2007), IL-1β (unpublished), and LTB4 (Monteiro et al., 2011). PubMed:24904418

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

a(CHEBI:heme) increases p(HGNC:IL1B) View Subject | View Object

Likewise, heme and FeNTA treatment causes the induction of the M1 markers MHCII, CD86, CD14, TNFα, IL-6, and IL1β and a decrease in the M2 markers CD206, IL-10, and Arginase-1 (the last with FeNTA only) in M0 BMDMs (Figure 3A; supplemental Figures 5, 6A, and 7). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Anemia, Sickle Cell
Text Location
Results

a(MESH:Monocytes) positiveCorrelation p(HGNC:IL1B) View Subject | View Object

For example, monocytes from SCD patients show an enhanced state of activation, with increased expression of interleukin (IL)-15 and production of TNFα and IL-1β. PubMed:26675351

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Introduction

bp(GO:"inflammatory response") positiveCorrelation p(HGNC:IL1B) View Subject | View Object

IL-1b participates in a robust inflammatory response. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

complex(a(CHEBI:heme), a(MESH:"ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate")) decreases p(HGNC:IL1B) View Subject | View Object

Cotreatment of M0 BMDMs with heme and TAK-242 attenuated the increase of the M1 markers MHCII, CD14, TNFα, IL-6, IL-1β, and CD86 and the decrease of the M2 marker CD206, IL-10, and Ym1 in comparison with heme treatment alone ( Figure 4A; supplemental Figures 5 and 12). PubMed:26675351

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Spleen
MeSH
Anemia, Sickle Cell
Text Location
Results

path(MESH:Fever) positiveCorrelation p(HGNC:IL1B) View Subject | View Object

Moreover, IL-1β and TNF modifies the hypothalamus threshold of the body temperature causing fever. PubMed:24904418

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

Out-Edges 26

act(p(HGNC:IL1B)) increases bp(GO:"neutrophil activation") View Subject | View Object

Caspase 1mediated activation of members of the IL-1β cytokine family leads to the recruitment and the activation of other immune cells, such as neutrophils, at the site of infection and/or tissue damage. PubMed:23702978

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

p(HGNC:IL1B) 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:IL1B) 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:IL1B) 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:IL1B) 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:IL1B) 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:IL1B) 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:IL1B) 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

sec(p(HGNC:IL1B)) increases p(HGNC:APP) View Subject | View Object

NO can also bring about apoptosis of hippocampal neurons via caspase- 3 activity [50] whereas astrocyte-secreted IL-1 beta can increase the production of APP and A beta from neu- rons [51–53] (Fig. 1). PubMed:27314526

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

sec(p(HGNC:IL1B)) increases a(CHEBI:"amyloid-beta") View Subject | View Object

NO can also bring about apoptosis of hippocampal neurons via caspase- 3 activity [50] whereas astrocyte-secreted IL-1 beta can increase the production of APP and A beta from neu- rons [51–53] (Fig. 1). PubMed:27314526

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

p(HGNC:IL1B) increases bp(GO:"neuron death") View Subject | View Object

Amyloid-β also induces microglial activation that results in NF-κB – induced expression of pro-inflammatory cytokines such as TNFα, IL1β, IL6, and IL8 from the microglia resulting in neuronal death PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:IL1B) 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:IL1B) increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

Nuclear local- ization of NF-κB in differentiated neuron progenitor cells (NPCs) is in- creasing following exposure to IL-1β and TNF-α, strong inducers of the NF-κB pathway with increase in the phosphorylation of IKK and p65 while decrease in the level of IκB [32]. PubMed:27288790

Appears in Networks:

p(HGNC:IL1B) increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

Then the stimulation of RAGE is able to activate the mitogen-activated protein kinase signaling cascades which converge in IκB kinase complex to phosphorylate IκB, thereby release and activate NF-κB, thus trigger NF-κB dependent gene transcription including IL-1β and TNF-α, which in turn induce the translocation of NF-κB to the nucleus [50]. PubMed:27288790

Appears in Networks:

p(HGNC:IL1B) increases p(FPLX:"IKK_complex", pmod(Ph)) View Subject | View Object

Nuclear local- ization of NF-κB in differentiated neuron progenitor cells (NPCs) is in- creasing following exposure to IL-1β and TNF-α, strong inducers of the NF-κB pathway with increase in the phosphorylation of IKK and p65 while decrease in the level of IκB [32]. PubMed:27288790

Appears in Networks:

p(HGNC:IL1B) increases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

Nuclear local- ization of NF-κB in differentiated neuron progenitor cells (NPCs) is in- creasing following exposure to IL-1β and TNF-α, strong inducers of the NF-κB pathway with increase in the phosphorylation of IKK and p65 while decrease in the level of IκB [32]. PubMed:27288790

Appears in Networks:

p(HGNC:IL1B) decreases p(FPLX:IKB) View Subject | View Object

Nuclear local- ization of NF-κB in differentiated neuron progenitor cells (NPCs) is in- creasing following exposure to IL-1β and TNF-α, strong inducers of the NF-κB pathway with increase in the phosphorylation of IKK and p65 while decrease in the level of IκB [32]. PubMed:27288790

Appears in Networks:

p(HGNC:IL1B) increases a(MESH:Cytokines) View Subject | View Object

Inhibition of NF-κB leads to decreased induction of cytokines and chemokines by IL-1β and TNF-α. PubMed:27288790

Appears in Networks:

p(HGNC:IL1B) increases a(MESH:Chemokines) View Subject | View Object

Inhibition of NF-κB leads to decreased induction of cytokines and chemokines by IL-1β and TNF-α. PubMed:27288790

Appears in Networks:

p(HGNC:IL1B) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Increased presence of NF-κB mediated IL-1β, IL-6, and TNF-α cytokines have been reported in the affected tissues, serum and CSF of AD patients PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:IL1B) positiveCorrelation bp(GO:"inflammatory response") View Subject | View Object

IL-1b participates in a robust inflammatory response. PubMed:24464629

Appears in Networks:
Annotations
MeSH
Kidney
Text Location
Introduction

p(HGNC:IL1B) positiveCorrelation path(MESH:Fever) View Subject | View Object

Moreover, IL-1β and TNF modifies the hypothalamus threshold of the body temperature causing fever. PubMed:24904418

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

p(HGNC:IL1B) increases path(MESH:Inflammation) View Subject | View Object

Although KC and IL-1β functions were not investigated during heme-induced inflammatory effects, TNF and LTB4 were described as essential inflammatory mediators during inflammatory events induced by heme. PubMed:24904418

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

p(HGNC:IL1B) increases path(MESH:Inflammation) View Subject | View Object

Pro-inflammatory cytokines and chemokines [e.g., inter leukin 1B (IL1B), CXCL8 (also termed IL8), TNF and chemokine (C-C motif) ligand 2 (CCL2, also termed MCP1)], are upregulated in haemolytic disorders such as SCD (Qari et al, 2012). This pro-inflammatory cytokine milieu is crucial in mediating the pro-coagulant effects of vascular endothelial cells and promotes localized inflammation and thrombosis (Qari et al, 2012). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

p(HGNC:IL1B) increases path(MESH:Thrombosis) View Subject | View Object

Pro-inflammatory cytokines and chemokines [e.g., inter leukin 1B (IL1B), CXCL8 (also termed IL8), TNF and chemokine (C-C motif) ligand 2 (CCL2, also termed MCP1)], are upregulated in haemolytic disorders such as SCD (Qari et al, 2012). This pro-inflammatory cytokine milieu is crucial in mediating the pro-coagulant effects of vascular endothelial cells and promotes localized inflammation and thrombosis (Qari et al, 2012). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
endothelial cell
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

p(HGNC:IL1B) positiveCorrelation a(MESH:Monocytes) View Subject | View Object

For example, monocytes from SCD patients show an enhanced state of activation, with increased expression of interleukin (IL)-15 and production of TNFα and IL-1β. PubMed:26675351

Appears in Networks:
Annotations
MeSH
Anemia, Sickle Cell
Text Location
Introduction

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.