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p(HGNC:RELA, pmod(Ph))

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Entity

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

Appears in Networks 4

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

Anatabine lowers Alzheimer's Aβ production in vitro and in vivo 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

In-Edges 21

a(CHEBI:Anatabine) decreases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

We observed that anatabine inhibits basal STAT3 phosphorylation levels (Mann– Whitney U=0, Z=-2.882, P=0.004) and reduces the induction of p65 NFkB phosphorylation by TNFa (Mann–Whitney U=0, Z=-2.882, P=0.004) within this 15 min time-frame (Fig. 1) PubMed:23178521

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

a(CHEBI:Anatabine) decreases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

Under these culture conditions, anatabine also inhibited both STAT3 and p65 NFkB phosphorylation induced by TNFa (Fig. 2) PubMed:23178521

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Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

a(CHEBI:Anatabine) decreases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

A significant inhibition of STAT3 phosphorylation was observed with 600 mg/ml of anatabine (Mann–Whitney U=0, Z=-2.309, P=0.021) and with 800 mg/ml of anatabine (Mann–Whitney U=0, Z=-2.309, P=0.021) and a significant inhibition of p65 NFkB phosphorylation was observed with 600 mg/ml of anatabine (Mann–Whitney U=1.0, Z=-2.021, P=0.043) and with 800 mg/ml of anatabine (Mann–Whitney U=0,Z=-2.309, P=0.021) PubMed:23178521

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

a(CHEBI:Anatabine) decreases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

We observed that anatabine significantly suppressed the stimulation of p65 NFkB and STAT3 phosphorylation by LPS in microglia (Fig. 3) PubMed:23178521

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Cell Ontology (CL)
microglial cell

a(CHEBI:Anatabine) decreases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

Kruskal–Wallis test revealed that doses of anatabine significantly suppressed both LPS induced STAT3 phosphorylation (H=15.658, df=4, P=0.005) and p65 NFkB phosphorylation (H=14.150, df=4, P=0.007) in human microglia PubMed:23178521

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Annotations
Cell Ontology (CL)
microglial cell

a(CHEBI:Anatabine) decreases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

Similarly, LPS induced p65 NFkB phosphorylation in microglia was significantly inhibited with 10 mg/ml of anatabine (Mann–Whitney U=0, Z=-2.309, P=0.021), with 100 mg/ml of anatabine (Mann– Whitney U=0, Z=-2.309, P=0.021), with 300 mg/ml of anatabine (Mann–Whitney U=0, Z=-2.309, P=0.021) PubMed:23178521

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

a(CHEBI:Anatabine) decreases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

An inhibition of TNFa induced STAT3 (Mann–Whitney U=0, Z=-2.121, P=0.034), and p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.121, P=0.034) was observed in these cells following the anatabine treatment (Fig. 4) suggesting that anatabine may also mediate its anti-inflammatory activity independently of nicotinic acetylcholine receptor expression PubMed:23178521

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Annotations
Experimental Factor Ontology (EFO)
HEK293

a(CHEBI:Anatabine) decreases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

Anatabine appears to completely antagonize LPS induced STAT3 (Mann–Whitney U=0, Z=-3.077, P=0.002) and p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-3.077, P=0.002) in human mononuclear cells PubMed:23178521

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

a(CHEBI:lipopolysaccharide) increases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

An increased STAT3 (Mann–Whitney U=0, Z=-2.309, P=0.021) and p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.309, p=0.021) was observed in LPS treated microglia (Fig. 3) PubMed:23178521

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

a(CHEBI:lipopolysaccharide) increases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

We observed that anatabine significantly suppressed the stimulation of p65 NFkB and STAT3 phosphorylation by LPS in microglia (Fig. 3) PubMed:23178521

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

a(CHEBI:lipopolysaccharide) increases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

Similarly, LPS induced p65 NFkB phosphorylation in microglia was significantly inhibited with 10 mg/ml of anatabine (Mann–Whitney U=0, Z=-2.309, P=0.021), with 100 mg/ml of anatabine (Mann– Whitney U=0, Z=-2.309, P=0.021), with 300 mg/ml of anatabine (Mann–Whitney U=0, Z=-2.309, P=0.021) PubMed:23178521

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

a(CHEBI:lipopolysaccharide) increases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

Following a 24 h incubation with LPS, a significant stimulation of STAT3 (Mann– Whitney U=0, Z=-2.882, P=0.004) and p65 NFkB phosphorylation was observed (Mann–Whitney U=1, Z=-2.722, P=0.006) PubMed:23178521

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

a(CHEBI:stattic) decreases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

We found that stattic inhibited STAT3 phosphorylation (Mann–Whitney U=0, Z=-2.324, P=0.02) and also suppressed p65 NFkB phosphorylation (Mann–Whitney U¼0, Z¼2.324, P¼0.02) mimicking the effect of anatabine in SHSY5Y cells (Fig. 1) PubMed:23178521

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

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

Appears in Networks:

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

Following this 15 mins of stimulation with TNFa, an increased p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.309, P=0.021) without a noticeable increase in STAT3 phosphorylation (Mann–Whitney U=7, Z=-0.289, P=0.773) was observed compared to the control conditions (Fig. 1) PubMed:23178521

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

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

An increased in both STAT3 (Mann–Whitney U=0, Z=-2.309, P=0.021) and p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.309, P=0.021) was observed following 24 h of treatment with TNFa PubMed:23178521

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y

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

TNFa significantly stimulated STAT3 (Mann–Whitney U=0, Z=-2.309, P=0.021) and p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.309, P=0.021) PubMed:23178521

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
HEK293

a(CHEBI:Anatabine) decreases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

In addition, an inhibition of p65 NFκB phosphorylation was observed following treatment with anatabine in 7W CHO overexpressing APP (Fig. 6A), in HEK293 (Fig. 6B) and in human neuronal like SH-SY5Y cells (Fig. 6C) showing that anatabine can prevent NFκB activation in various cell lines. PubMed:21958873

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
CHO cell
Experimental Factor Ontology (EFO)
SH-SY5Y

a(CHEBI:berberine) decreases p(HGNC:RELA, pmod(Ph)) View Subject | View Object

Furthermore, berberine decreased the phosphorylation and expression of p65 [188]. PubMed:29179999

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:TNF) 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:

Out-Edges 0

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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.