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p(HGNC:IL1A)

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Entity

Name
IL1A
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 4

Activation and regulation of the inflammasomes v1.0.0

RelB/p50 complexes regulate cytokine-induced YKL-40 expression 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

In-Edges 3

complex(GO:"NF-kappaB complex") increases act(p(HGNC:IL1A)) View Subject | View Object

Moreover, NF-κB – induced IL1 genesis has been shown to precipitate tau phosphorylation at Ser202 and Thr205 (AT8 epitopes) via the activation of the p38- MAPK pathway PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:curcumin) decreases p(HGNC:IL1A) 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:14193399) decreases p(HGNC:IL1A) View Subject | View Object

Glaucocalyxin B, found in Rabdosia japonica, considerably atten-uated the expression of NO, TNF-, IL-1, COX-2 and iNOS in LPS-induced microglia cells [169–172]. Moreover, the activation of NF-B, p38 MAPK and ROS generation was interrupted by glauco- calyxin B in LPS-induced microglia cells [172]. PubMed:29179999

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

Out-Edges 6

p(HGNC:IL1A) increases act(p(HGNC:IL1R1)) View Subject | View Object

In addition, IL-1α, which also activates IL-1R, could contribute to the inflammatory response in vivo. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:IL1A) increases bp(GO:"inflammatory response") View Subject | View Object

In addition, IL-1α, which also activates IL-1R, could contribute to the inflammatory response in vivo. PubMed:23702978

Appears in Networks:
Annotations
Confidence
Medium
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:IL1A) increases p(HGNC:RELB) View Subject | View Object

Interestingly, although human astrocytes constitutively express low levels of RelB, IL-1 induced dramatic RelB protein accumulation in these cells (Fig. 4C). PubMed:25681350

Appears in Networks:
Annotations
Cell Ontology (CL)
astrocyte

p(HGNC:IL1A) causesNoChange r(HGNC:CHI3L1) View Subject | View Object

In contrast to astrocytes and U373 cells, we found that basal expression of YKL-40 and RelB mRNA was very high in primary human chondrocytes and not stimulated by IL-1 or OSM (Supplementary Fig 3). PubMed:25681350

Appears in Networks:
Annotations
Cell Ontology (CL)
chondrocyte

p(HGNC:IL1A) causesNoChange r(HGNC:RELB) View Subject | View Object

In contrast to astrocytes and U373 cells, we found that basal expression of YKL-40 and RelB mRNA was very high in primary human chondrocytes and not stimulated by IL-1 or OSM (Supplementary Fig 3). PubMed:25681350

Appears in Networks:
Annotations
Cell Ontology (CL)
chondrocyte

act(p(HGNC:IL1A)) increases bp(GO:"p38MAPK cascade") View Subject | View Object

Moreover, NF-κB – induced IL1 genesis has been shown to precipitate tau phosphorylation at Ser202 and Thr205 (AT8 epitopes) via the activation of the p38- MAPK pathway PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

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.