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p(HGNC:IL6)

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Entity

Name
IL6
Namespace
hgnc
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/hgnc-symbols.belns

Appears in Networks 6

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

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

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 24

a(HBP:HBP00089) increases sec(p(HGNC:IL6)) 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

bp(GO:"astrocyte activation") increases sec(p(HGNC:IL6)) 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:IL6)) 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

act(a(MESH:Microglia)) increases p(HGNC:IL6) 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") increases p(HGNC:IL6) View Subject | View Object

NF-κB positively regulates the transcription of interleukin 6 (IL6) family of cytokines such as IL6, leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) [184], which in-turn induce the differentiation of NSC into astrocytes by activating transcription factors STAT3, AP-1, and NF-κB itself PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(GO:"NF-kappaB complex") increases p(HGNC:IL6) View Subject | View Object

IL6 is another NF-κB – induced [256-260] pro-inflammatory cytokine up-regulated and integrally involved in the etio-pathogenesis of Alzheimer’s disease PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(GO:"NF-kappaB complex") increases p(HGNC:IL6) View Subject | View Object

Furthermore, NF-κB - induced IL6 has been demonstrated to evoke hyperphosphorylation of tau at Ser202 and Thr205 via the activation of the cdk5/p35 complex PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(GO:"NF-kappaB complex") increases p(HGNC:IL6) 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

path(MESH:"Alzheimer Disease") association p(HGNC:IL6) View Subject | View Object

IL6 is another NF-κB – induced [256-260] pro-inflammatory cytokine up-regulated and integrally involved in the etio-pathogenesis of Alzheimer’s disease PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"1,8-cineole") decreases p(HGNC:IL6) 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:"alpha-tocopherol") decreases p(HGNC:IL6) 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:

a(CHEBI:"amyloid-beta") increases sec(p(HGNC:IL6)) 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:curcumin) decreases p(HGNC:IL6) View Subject | View Object

Curcumin showed several anti-inflammatory characteristics. It deploys various cytokine-inhibitory, anti-inflammatory activities and decreases the expression levels of COX-2, LOX, and iNOS. Moreover, the expression of the pro-inflammatory cytokines, for instance, TNF-, IL-1, -2,-6, -8, and -12 and the neurotoxic factors were suppressed by curcumin in lipopolysaccharide (LPS)-stimulated monocytes and alveolar macrophages [103]. PubMed:29179999

Appears in Networks:

a(PUBCHEM:444795) decreases p(HGNC:IL6) View Subject | View Object

Retinoic acid showed anti-inflammatory qualities via suppressing the expression of the inflammatory mediators IL-6, IL-12 and TNF- [216–219] and mod-ulating NF-B signaling [220,221]. PubMed:29179999

Appears in Networks:

complex(GO:"NF-kappaB complex") increases p(HGNC:IL6) 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:IL6) 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:"N-acetyl-L-cysteine") decreases p(HGNC:IL6) View Subject | View Object

Similarly, NAC prevented increased expression of MHCII, CD14, TNFα, IL-6, IL-1β, and CD86 and mildly compensated for the decrease of CD206 and IL-10 following heme treatment (Figure 4D; supplemental Figure 5). PubMed:26675351

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

a(CHEBI:heme) increases p(HGNC:IL6) View Subject | View Object

Moreover, heme amplifies MyD88- (TNF and IL-6) and TRIF-dependent (IP-10) cytokines. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Malaria
Text Location
Review

a(CHEBI:heme) increases p(HGNC:IL6) View Subject | View Object

In addition, we observed increased ROS production ( Figure 2I; supplemental Figure 2), as well as an enhanced expression of IL-6 and TNFα in cells treated with heme-albumin compared with heme-Hx (Figure 2J-K). PubMed:26675351

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

a(CHEBI:heme) increases p(HGNC:IL6) 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:"ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate") decreases p(HGNC:IL6) View Subject | View Object

In hepatic macrophages, TAK-242 also diminished heme-driven induction of IL-6 and TNFα and NAC partially recovered CD206 downregulation ( Figure 5B-C). PubMed:26675351

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

complex(a(CHEBI:heme), a(MESH:"ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate")) decreases p(HGNC:IL6) 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

complex(a(CHEBI:heme), a(MESH:Lipopolysaccharides)) increases p(HGNC:IL6) View Subject | View Object

In vivo, injection of heme and LPS induces a significant increase in the concentrations of TNF and IL-6 when compared to the challenge with LPS alone (Fernandez et al., 2010). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Liver
MeSH
Cerebral Hemorrhage
Text Location
Review

p(HGNC:AMBP) increases p(HGNC:IL6) View Subject | View Object

Treatment with A1M led to a small, non-significant, transient increase in plasma interleukin 6 24 hours after the first injection. PubMed:24489717

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Kidney Tubules, Proximal
Text Location
Results

Out-Edges 8

p(HGNC:IL6) increases bp(GO:"astrocyte development") View Subject | View Object

NF-κB positively regulates the transcription of interleukin 6 (IL6) family of cytokines such as IL6, leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) [184], which in-turn induce the differentiation of NSC into astrocytes by activating transcription factors STAT3, AP-1, and NF-κB itself PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:IL6) increases p(HGNC:STAT3) View Subject | View Object

NF-κB positively regulates the transcription of interleukin 6 (IL6) family of cytokines such as IL6, leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) [184], which in-turn induce the differentiation of NSC into astrocytes by activating transcription factors STAT3, AP-1, and NF-κB itself PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:IL6) increases a(MESH:"Transcription Factor AP-1") View Subject | View Object

NF-κB positively regulates the transcription of interleukin 6 (IL6) family of cytokines such as IL6, leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) [184], which in-turn induce the differentiation of NSC into astrocytes by activating transcription factors STAT3, AP-1, and NF-κB itself PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:IL6) increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

NF-κB positively regulates the transcription of interleukin 6 (IL6) family of cytokines such as IL6, leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF) [184], which in-turn induce the differentiation of NSC into astrocytes by activating transcription factors STAT3, AP-1, and NF-κB itself PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:IL6) association path(MESH:"Alzheimer Disease") View Subject | View Object

IL6 is another NF-κB – induced [256-260] pro-inflammatory cytokine up-regulated and integrally involved in the etio-pathogenesis of Alzheimer’s disease PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:IL6) increases p(HGNC:MAPT, pmod(Ph, Ser, 202), pmod(Ph, Thr, 205)) View Subject | View Object

Furthermore, NF-κB - induced IL6 has been demonstrated to evoke hyperphosphorylation of tau at Ser202 and Thr205 via the activation of the cdk5/p35 complex PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:IL6) 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:IL6) 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

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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.