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p(HGNC:STAT3, pmod(Ph))

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Entity

Name
STAT3
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 4

Nicotinic acetylcholine receptor signalling: roles in Alzheimer's disease and amyloid neuroprotection. v1.0.0

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

Chronic Anatabine Treatment Reduces Alzheimer ’ s Disease (AD)-Like Pathology and Improves Socio-Behavioral Deficits in a Transgenic Mouse Model of AD v1.0.0

Phytochemicals as inhibitors of NF-κB for treatment of Alzheimer’s disease v1.0.0

In-Edges 23

act(a(CHEBI:nicotine)) increases p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

Nicotine induced phosphorylation of STAT-3 (signal transducer and activator of transcription 3) in peritoneal macrophages is mediated by an alpha7-dependent activation of JAK-2, as part of the anti-inflammatory action of vagal nerve stimulation (de Jonge et al., 2005). PubMed:19293145

Appears in Networks:
Annotations
Cell Ontology (CL)
peritoneal macrophage

composite(p(FPLX:JAK), p(HGNC:STAT3)) increases p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

Paradoxically, Abeta also activates the MAPK pathway through an alpha7-dependent pathway (Dineley et al., 2001; Bell et al., 2004). In human oral keratinocytes, the Ras/Raf/mitogen-activated protein kinase kinase 1/ERK pathway cooperates with the nicotine activation of the JAK/STAT-3 pathway (Arredondo et al., 2006); the Ras pathway induces STAT-3 upregulation whereas the JAK/STAT-3 pathway phosphorylates STAT-3. PubMed:19293145

Appears in Networks:

p(HGNC:STAT3) hasVariant p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

Appears in Networks:

a(CHEBI:Anatabine) decreases p(HGNC:STAT3, 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:STAT3, 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

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

a(CHEBI:Anatabine) decreases p(HGNC:STAT3, 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:STAT3, 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:Anatabine) decreases p(HGNC:STAT3, 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

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

a(CHEBI:Anatabine) decreases p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

A significant inhibition of STAT3 phosphorylation was observed with 10 mg/ml of anatabine (Mann–Whitney U=1, Z=-2.021, P=0.043), 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) and with 600 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:STAT3, 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

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

a(CHEBI:Anatabine) decreases p(HGNC:STAT3, 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:STAT3, 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:STAT3, 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:STAT3, 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:nicotine) association p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

Nicotine has been shown to modulate inflammation by affecting STAT3 phosphorylation (Chatterjee et al., 2009; Hosur and Loring, 2011) and by opposing NFkB activation (Leite et al., 2010; Zhou et al., 2010) PubMed:23178521

Appears in Networks:

a(CHEBI:stattic) decreases p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

As a positive control, we used stattic, a known inhibitor of STAT3 dimerization and phosphorylation PubMed:23178521

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

a(CHEBI:stattic) decreases p(HGNC:STAT3, 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:TNF) causesNoChange p(HGNC:STAT3, 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:STAT3, 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:STAT3, 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:"amyloid-beta") increases p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

We ob- served an elevation of STAT3 phosphorylation in the hippocampus and cortex of Tg PS1/ APPswe compared to their control wild-type littermates (Fig 6A). PubMed:26010758

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

a(CHEBI:Anatabine) decreases p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

A significant reduction in STAT3 phosphorylation was observed in the hippocampus and cortex of Tg PS1/APPswe mice treated with 10 or 20 mg/Kg/Day of anatabine compared to Tg PS1/APPswe receiving regular drinking water (Fig 6B) showing that anatabine prevents STAT3 activation in the brain of Tg PS1/APPswe mice. PubMed:26010758

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus
MeSH
Alzheimer Disease

a(CHEBI:resveratrol) decreases p(HGNC:STAT3, pmod(Ph)) View Subject | View Object

Resveratrol disrupted the phosphorylation of signal transducer and activator of transcription factor 1 (STAT1) and STAT3 [115]. PubMed:29179999

Appears in Networks:

Out-Edges 1

p(HGNC:STAT3, pmod(Ph)) association a(CHEBI:nicotine) View Subject | View Object

Nicotine has been shown to modulate inflammation by affecting STAT3 phosphorylation (Chatterjee et al., 2009; Hosur and Loring, 2011) and by opposing NFkB activation (Leite et al., 2010; Zhou et al., 2010) PubMed:23178521

Appears in Networks:

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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.