1. Catalog
  2. Nodes
  3. p(HGNC:NOS2)

p(HGNC:NOS2)

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

Entity

Name
NOS2
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 6

Activation and regulation of the inflammasomes v1.0.0

Inflammasome Involvement in Alzheimer’s Disease v1.0.0

Anatabine ameliorates experimental autoimmune thyroiditis. 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

In-Edges 17

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

bp(GO:"astrocyte activation") increases sec(p(HGNC:NOS2)) 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:NOS2)) 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

a(CHEBI:Anatabine) decreases 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: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:

a(CHEBI:"1,8-cineole") decreases p(HGNC:NOS2) View Subject | View Object

Further-more, the expression of NOS-2, COX2 and NF-B was reduced by1,8-cineole [250]. PubMed:29179999

Appears in Networks:

a(CHEBI:"alpha-tocopherol") decreases p(HGNC:NOS2) 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:curcumin) decreases p(HGNC:NOS2) 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(CHEBI:resveratrol) decreases p(HGNC:NOS2) View Subject | View Object

It also lowered the expression of NO and iNOS, and prostaglandin E2 (PGE2) and COX2 in A-activated glial cells. All these effects were attributableto their suppression of nuclear NF-B translocation [116]. PubMed:29179999

Appears in Networks:

a(PUBCHEM:102336202) decreases p(HGNC:NOS2) View Subject | View Object

It down-regulated iNOS expression and nitrotyrosin levels in the hip-pocampus and stimulated the mRNA expression level of IL-4 [247]. PubMed:29179999

Appears in Networks:
Annotations
MeSH
Hippocampus

a(PUBCHEM:14193399) decreases p(HGNC:NOS2) 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

a(PUBCHEM:164676) decreases act(p(HGNC:NOS2)) View Subject | View Object

It inhibited the activation of iNOS, matrix metalloproteinase 2 (MMP2), and NF-Bp65 and consequently prevent AD in the brain [229–231]. PubMed:29179999

Appears in Networks:

a(PUBCHEM:440312) decreases p(HGNC:NOS2) View Subject | View Object

LPS-activated expression of pro-inflammatory and neurotoxic factors like NO, TNF-, PGE2, NO synthase and COX2 production and LOX activity were inhibited by dihydroasparagusic acid in microglia cells [243]. PubMed:29179999

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

a(CHEBI:"(+)-Tetrandrine") decreases p(HGNC:NOS2) View Subject | View Object

Tetrandrine, is an herb-derived bisbenzylioquinoline alkaloid, may be a potent inhibitor of NF-κB activation and can inhibit the expression of iNOS and COX-2 which are involved in pro-inflammation. PubMed:27288790

Appears in Networks:

p(FPLX:NFkappaB) regulates act(p(HGNC:NOS2)) View Subject | View Object

ROS has been found not only the regulators of NF-κB, interestingly, iNOS is also regulated by NF-κB. PubMed:27288790

Appears in Networks:

act(complex(GO:"NF-kappaB complex")) increases act(p(HGNC:NOS2)) View Subject | View Object

Excessive accumulation of Aβ1-42 stimulates microglial cells by signaling via receptor associated advanced glycation end products (RAGE) and peroxisome proliferator-activated receptor-γ (PPAR-γ), phosphorylates IKK proteins, and enhances NF-κB mediated transactivation of inflammatory cytokines and neurotoxic molecules such as glutamate and reactive oxygen species (ROS)/induced nitric oxide synthase (iNOS) [12] (Fig 2B) PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(complex(GO:"NF-kappaB complex")) increases act(p(HGNC:NOS2)) View Subject | View Object

Furthermore NF-κB specific inhibitor prevents iNOS and ROS upregulation in Aβ stimulated cultures of astrocytes or mixed cortical cells PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

Out-Edges 3

act(p(HGNC:NOS2)) increases a(CHEBI:"nitric oxide") 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

act(p(HGNC:NOS2)) increases a(CHEBI:"nitric oxide") 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:NOS2) increases path(MESH:Inflammation) View Subject | View Object

Tetrandrine, is an herb-derived bisbenzylioquinoline alkaloid, may be a potent inhibitor of NF-κB activation and can inhibit the expression of iNOS and COX-2 which are involved in pro-inflammation. PubMed:27288790

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.