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p(HGNC:IFNG)

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

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

Appears in Networks 4

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

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

Activation and regulation of the inflammasomes v1.0.0

Anatabine ameliorates experimental autoimmune thyroiditis. v1.0.0

In-Edges 2

a(HBP:HBP00089) increases sec(p(HGNC:IFNG)) 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(GO:"neurofibrillary tangle") increases p(HGNC:IFNG) 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

Out-Edges 6

p(HGNC:IFNG) increases p(HGNC:AIM2) View Subject | View Object

In addition, AIM2 expression can be induced by IFNβ and IFNγ65,66. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph

p(HGNC:IFNG) decreases act(p(HGNC:NLRP3)) View Subject | View Object

In addition, T cell-derived IFNγ has been shown to downregulate the activity of NLRP3 via activation of inducible nitric oxide synthase (iNOS) in a mouse model of tuberculosis71; nitric oxide (NO) induces NLRP3 nitrosylation and thereby inhibits NLRP3 activity. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interferon signaling subgraph
NeuroMMSigDB
Nitric oxide subgraph

p(HGNC:IFNG) increases act(p(HGNC:NOS2)) View Subject | View Object

In addition, T cell-derived IFNγ has been shown to downregulate the activity of NLRP3 via activation of inducible nitric oxide synthase (iNOS) in a mouse model of tuberculosis71; nitric oxide (NO) induces NLRP3 nitrosylation and thereby inhibits NLRP3 activity. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Caspase subgraph
NeuroMMSigDB
Interferon signaling subgraph
NeuroMMSigDB
Nitric oxide subgraph

p(HGNC:IFNG) increases p(HGNC:CARD17) 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

p(HGNC:IFNG) increases p(HGNC:NOS2) View Subject | View Object

Anatabine suppressed in a dose- dependent manner the increase of iNOS and COX2 in- duced by interferon-g (Fig.4),confirming in vitro its antiinflammatory properties. The effect seen with inter- feron-g was also seen when macrophages were stimulated with lipopolysaccharide (Supplemental Fig. 1). PubMed:22807490

Appears in Networks:

p(HGNC:IFNG) increases p(HGNC:PTGS2) View Subject | View Object

Anatabine suppressed in a dose- dependent manner the increase of iNOS and COX2 in- duced by interferon-g (Fig.4),confirming in vitro its antiinflammatory properties. The effect seen with inter- feron-g was also seen when macrophages were stimulated with lipopolysaccharide (Supplemental Fig. 1). PubMed:22807490

Appears in Networks:

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.