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p(FPLX:NFkappaB)

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Entity

Name
NFkappaB
Namespace
FPLX
Namespace Version
20180917
Namespace URL
https://raw.githubusercontent.com/sorgerlab/famplex/e8ae9926ff95266032cb74f77973c84939bffbeb/export/famplex.belns

Appears in Networks 9

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

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Anatabine ameliorates experimental autoimmune thyroiditis. 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

Screening of a neuronal cell model of Tau pathology for therapeutic compounds v1.0.0

Increased NF-κB signalling up-regulates BACE1 expression and its therapeutic potential in Alzheimer's disease. 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 82

bp(GO:"MAPK cascade") increases act(p(FPLX:NFkappaB)) View Subject | View Object

Nicotine also activates ERK in non-neuronal cells such as pancreatic acinar cells (Chowdhury et al., 2007) and vascular smooth muscle cells (Kanda and Watanabe, 2007), although it is not known in those cases which nAChR subtypes are involved. In the cortex and hippocampus of mice, nicotine’s inhibition of MAPK (shown by RNAi reduction of alpha7 expression to be alpha7-dependent) prevents activation of nuclear factor- kappaB and c-Myc, also thereby reducing the activity of inducible nitric-oxide synthetase and NO production and decreasing Abeta production (Liu et al., 2007). PubMed:19293145

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Annotations
Cell Ontology (CL)
pancreatic acinar cell
Cell Ontology (CL)
vascular associated smooth muscle cell

a(CHEBI:nicotine) decreases act(p(FPLX:NFkappaB)) 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(HBP:"Chronic cerebral hypoperfusion") increases p(FPLX:NFkappaB) View Subject | View Object

Chronic Brain hypoperfusion (CBH) elevates nuclear factor-kB (NF-kB), which binds with the promoter sequences of miR-195 and negatively regulates its expression. Down-regulated miR-195 up-regulates APP and BACE1 and increases Aß levels. Some Aß then enter the intracellular space and activate calpain, promoting the conversion of Cdk5/p35 to Cdk5/p25 and catalyzes the degradation of IkB (inhibitor of NF-?B)and directly phosphorylates Tau. Down-regulated miR-195 up-regulates p35, which provides the active substrates of p25 PubMed:26118667

Appears in Networks:

complex(g(MIRBASE:"rno-mir-195"), p(FPLX:NFkappaB)) hasComponent p(FPLX:NFkappaB) View Subject | View Object

Appears in Networks:

a(CHEBI:Anatabine) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Furthermore, anatabine has been recently shown to inhibit nuclear factor-kB(NF-kB) activation and reduce neuroinflammation in a mouse model of Alzheimer disease (15). PubMed:22807490

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"amyloid-beta") increases act(p(FPLX:NFkappaB)) View Subject | View Object

We also observed elevation of NFκB activation in the vicinity of Aβ deposits in the brain of Tg PS1/APPswe mice (Fig 7A). PubMed:26010758

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Alzheimer Disease

a(CHEBI:Anatabine) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

We have shown previously that anatabine displays some anti-inflammatory properties by reducing the activation of NFκB and STAT3 [17,18]. PubMed:26010758

Appears in Networks:

a(CHEBI:Anatabine) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

We have previously shown that anatabine inhibits STAT3 and NFκB activation [18] resulting in decreased neuroinflammation in a mouse model of multiple sclerosis. PubMed:26010758

Appears in Networks:
Annotations
MeSH
Multiple Sclerosis

a(CHEBI:Anatabine) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Interestingly, we found a significant reduction in the expression of amyloid plaque associated phospho-p65 NFκB immunopositive cells in Tg PS1/APPswe mice treated with anatabine at either 10 or 20 mg/Kg/Day (Fig 7B) showing that anatabine prevents NFκB activation in the brain of Tg PS1/APPswe mice. PubMed:26010758

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Alzheimer Disease

a(PUBCHEM:5318517) association p(FPLX:NFkappaB) View Subject | View Object

Tab. 1A-B: Summary of the Tau aggregation modulators (inhibitors = 18 (A), stimulators = 10 (B)) which show decrease / increase in the amount of ThS + cells without affecting the expression level of TauRD∆K compared to the compound untreated control. PubMed:30640040

Appears in Networks:

complex(g(HGNC:BACE1), p(FPLX:NFkappaB)) hasComponent p(FPLX:NFkappaB) View Subject | View Object

Appears in Networks:

p(HGNC:TNF) increases act(p(FPLX:NFkappaB), ma(tscript)) View Subject | View Object

Our data clearly demonstrate that NSAIDs inhibit TNF-a-induced BACE1 transcription via its NF-kB cis-acting elements. PubMed:21329555

Appears in Networks:

a(CHEBI:"(+)-artemisinin") decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Moreover,it reveals promising anti-inflammatory actions through suppress-ing the activation of NF-B [238–240]. PubMed:29179999

Appears in Networks:

a(CHEBI:"1,8-cineole") decreases p(FPLX:NFkappaB) 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:"N(5)-ethyl-L-glutamine") decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Besides, extracellular signal-regulated kinase (ERK), p38 MAPK and NF-B pathway were disrupted byL-theanine [128]. PubMed:29179999

Appears in Networks:

a(CHEBI:"alpha-tocopherol") decreases act(p(FPLX:NFkappaB)) 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:"amyloid-beta") increases act(p(FPLX:NFkappaB)) View Subject | View Object

Furthermore, A induced NF-B activity in glial and neuronal cells. NF-B is involved in inflammatory responses and is expressed in brains of AD patients [32]. PubMed:29179999

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

a(CHEBI:"gallic acid") decreases act(p(FPLX:NFkappaB)) View Subject | View Object

A-activated NF-B activity and the expression of cytokines were attenuated with gallic acid in microglial cells y decreased acetylation of RelA, which subsequently reduced A-activated neu-rotoxicity [164]. PubMed:29179999

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

a(CHEBI:"reactive oxygen species") increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

ROS activate various downstream signaling molecules, such as PKC and mitogen-activated protein kinases (MAPKs) that induce nuclear translocation of NF-B and the expression of pro-inflammatory genes [41]. PubMed:29179999

Appears in Networks:

a(CHEBI:Anatabine) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Anatabine lowered NF-B activation by inhibiting A production in vitro [195]. PubMed:29179999

Appears in Networks:

a(CHEBI:Geniposide) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Geniposide considerably suppressed RAGE-related signaling such as ERK and IB/NF-B, the expression of TNF-, IL-1 and cerebral A accumulation in vivo[245] PubMed:29179999

Appears in Networks:

a(CHEBI:curcumin) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Inhibition of the NF-B pathway represents a well-defined anti-inflammatory mechanism of curcumin[104,105]. Curcumin inhibited the phosphorylation and degrada-tion of IB and the nuclear translocation of NF-B p65 [106]. PubMed:29179999

Appears in Networks:

a(CHEBI:galanthamine) increases act(p(FPLX:NFkappaB)) View Subject | View Object

The protective effects of galantamine in brain microvascular endothelial cells were mediated via protective gene, heme oxygenase-1 induction through NF-B activation [168] PubMed:29179999

Appears in Networks:

a(CHEBI:genistein) decreases p(FPLX:NFkappaB) View Subject | View Object

Pretreatment with genistein significantly alleviated A 25-35-stimulated TLR4 and NF-B expres-sion, DNA binding and NF-B activities[159]. PubMed:29179999

Appears in Networks:

a(CHEBI:genistein) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Pretreatment with genistein significantly alleviated A 25-35-stimulated TLR4 and NF-B expres-sion, DNA binding and NF-B activities[159]. PubMed:29179999

Appears in Networks:

a(CHEBI:oridonin) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

It inhibited the activation of NF-B in TNF- induced HepG2 cells [193]. PubMed:29179999

Appears in Networks:

a(CHEBI:pterostilbene) regulates p(FPLX:NFkappaB) View Subject | View Object

It is even more potent than resveratrol through PPAR regulation [118,119], NF-B transcription[120–122] and JNK phosphorylation [123,124]. PubMed:29179999

Appears in Networks:

a(CHEBI:resveratrol) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Besides, it decreased the phosphorylation of IKK and IB through LPS stimulation and subse-quently inhibited the activity of NF-B [115]. PubMed:29179999

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a(PUBCHEM:102336202) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Xanthoceraside decreased the expression of A 25-35/IFN--stimulated NO, IL-1,and TNF- in microglia, which implicated the down-regulation of the activities of MAPK and NF-B pathways [248] PubMed:29179999

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

a(PUBCHEM:14193399) decreases act(p(FPLX:NFkappaB)) 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:155160) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

It inactivated– and -secretases and astrocytes through the inter-ference of NF-B activation [144 PubMed:29179999

Appears in Networks:

a(PUBCHEM:164676) decreases p(FPLX:NFkappaB) View Subject | View Object

Tanshinone IIA reduced the glial fibrillary acidic protein (GFAP) and NF-B and induced the expression of neuronal nuclear antigen (NeuN), Nissl bodies, and IB in AD [235,236]. PubMed:29179999

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(PUBCHEM:24721561) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Ginsenoside Rd showed neuro-protective effects with A 40 activated impairments in rat brains [225] and ameliorated learning and memory capability in APP transgenic mice, via reducing the activity of NF-B [226]. PubMed:29179999

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(PUBCHEM:440312) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Besides, it significantly decreased the generation of ROS and affected LPS-induced activation of MAPK, including p38 and NF-B signaling[243]. PubMed:29179999

Appears in Networks:

a(PUBCHEM:441923) decreases p(FPLX:NFkappaB) View Subject | View Object

The expression of the protein and mRNA of TLR3, TLR4, NF-B and TNF receptor associated factor 6 (TRAF-6) were substantially decreased by ginsenoside Rg1, and it also decreased the expression of TNF- and IFN- [227] PubMed:29179999

Appears in Networks:

a(PUBCHEM:442534) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

It attenuated the development of AD by inhibiting glycogen synthase kinase 3 (GSK-3) and NF-B activation, and sup-pressing the NLRP3 inflammasome and cytokines such as TNF-and IL-1 [1]. PubMed:29179999

Appears in Networks:

a(PUBCHEM:444795) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Retinoic acid showed anti-inflammatory qualities via suppressing the expression of the inflammatory mediators IL-6, IL-12 and TNF- [216–219] and mod-ulating NF-B signaling [220,221]. PubMed:29179999

Appears in Networks:

a(PUBCHEM:444795) decreases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

It reduced BACE1 expression and repressed LPS-activated nuclear translocation of NF-B and its binding to the BACE1 promoter [222]. PubMed:29179999

Appears in Networks:

a(PUBCHEM:73078) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Tetrandrine inhibited the activity of NF-B and down-regulated the expression of pro-inflammatory cytokines [178–180]. PubMed:29179999

Appears in Networks:

a(PUBCHEM:73078) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

It ameliorated spatial learning and memory disorder, which was caused by A 1-42 and was associated with the inter-ference of NF-B activity and the inhibition of IL-1 and TNF-expression [183]. PubMed:29179999

Appears in Networks:

bp(GO:"inflammatory response") association act(p(FPLX:NFkappaB)) View Subject | View Object

Furthermore, A induced NF-B activity in glial and neuronal cells. NF-B is involved in inflammatory responses and is expressed in brains of AD patients [32]. PubMed:29179999

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

complex(a(MESH:DNA), p(FPLX:NFkappaB)) hasComponent p(FPLX:NFkappaB) View Subject | View Object

Appears in Networks:

p(HGNC:NFKBIA) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

It inhibited the degradation of IkBa, a cytoplasmic NF-B inhibitor, and p65translocation to the nucleus by disabling IkBa alpha kinase beta and  activiies [181,182]. PubMed:29179999

Appears in Networks:

p(HGNC:TNF) increases act(p(FPLX:NFkappaB)) View Subject | View Object

It inhibited the activation of NF-B in TNF- induced HepG2 cells [193]. PubMed:29179999

Appears in Networks:

path(HP:Neurodegeneration) association act(p(FPLX:NFkappaB)) View Subject | View Object

Degeneration of neurons in the brain of AD patients is associated with the activation of NF-B [7 PubMed:29179999

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

path(MESH:"Alzheimer Disease") positiveCorrelation p(FPLX:NFkappaB) View Subject | View Object

Furthermore, A induced NF-B activity in glial and neuronal cells. NF-B is involved in inflammatory responses and is expressed in brains of AD patients [32]. PubMed:29179999

Appears in Networks:
Annotations
MeSH
Brain

a(CHEBI:"(+)-Tetrandrine") decreases act(p(FPLX:NFkappaB)) 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:

a(CHEBI:"amyloid-beta") increases act(p(FPLX:NFkappaB)) View Subject | View Object

In cell models triggering supraphysiological concentrations of Aβ pep- tides, NF-κB is activated, as well as in both neuronal cells and microglial cells, showing that NF-κB pathway has been linked to Aβ neurotoxicity [14]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Microglia
MeSH
Neurons

a(CHEBI:"hydrogen peroxide") increases act(p(FPLX:NFkappaB)) View Subject | View Object

Previous find- ings have identified ROS as a common denominator of NF-κB activating signals, as Chetsawang B found that NF-κB was increased in H 2 O 2 -treat- ed SH-SY5Y cells [22,23]. PubMed:27288790

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

a(CHEBI:"reactive oxygen species") increases act(p(FPLX:NFkappaB)) View Subject | View Object

Previous find- ings have identified ROS as a common denominator of NF-κB activating signals, as Chetsawang B found that NF-κB was increased in H 2 O 2 -treat- ed SH-SY5Y cells [22,23]. PubMed:27288790

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

a(CHEBI:"reactive oxygen species") regulates act(p(FPLX:NFkappaB)) 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

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a(CHEBI:hydroxytyrosol) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Hydroxytyrosol is an orally bioavailable polyphenol, obtained from ol- ives, which inhibits NF-κB activity and has elicited promising efficacy signals in several inflammatory diseases [88]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

a(CHEBI:melatonin) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

The antioxidants LY231617, and melatonin pro- tect the neurons against the insult and prevented the Tyr42 phosphorylation of IκBα, which acts to protect the neurons against physiological injury by repressing the insult-induced oxidative stress activation of transcription factor NF-κB [86]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

a(MESH:Lipopolysaccharides) increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

LPS treatment induced the nuclear translocation of NF-κB and increased the expression and secretion of TNF-α and IL-1β [63]. PubMed:27288790

Appears in Networks:

a(MESH:Morphine) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

The activity of NF-κB in the cell models was strongly inhibited by morphine, which was achieved by a marked up-regulation of the inhibitor of IκB. PubMed:27288790

Appears in Networks:

a(PUBCHEM:3968) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

The antioxidants LY231617, and melatonin pro- tect the neurons against the insult and prevented the Tyr42 phosphorylation of IκBα, which acts to protect the neurons against physiological injury by repressing the insult-induced oxidative stress activation of transcription factor NF-κB [86]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

a(PUBCHEM:439378) decreases p(FPLX:NFkappaB) View Subject | View Object

L-Theanine, an amino acid in green tea, reduced Aβ 42 levels in the cortex and hippocampus of the brain, which is mediated by suppres- sion of ERK/p38 and NF-κB as well as the reduction of macromolecular oxidative damage [81]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

a(PUBCHEM:6440944) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

Omega-6 phospholipids, e.g. dilinoleoylphosphatidylcholine (DLPC), have been shown to block TNF-α and H 2 O 2 activation of MAPK as well as blocks IκBα phosphorylation in the SH-SY5Y cells and prevents the phosphorylation and activation of NF-κB. PubMed:27288790

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
SH-SY5Y
MeSH
Cerebral Cortex
MeSH
Hippocampus

bp(GO:"ERK1 and ERK2 cascade") increases act(p(FPLX:NFkappaB)) View Subject | View Object

Evidence has shown that NF-κB can be activated by ERK pathway [44]. PubMed:27288790

Appears in Networks:

bp(GO:"apoptotic process") association p(FPLX:NFkappaB) View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

bp(GO:"negative regulation of neuron apoptotic process") association p(FPLX:NFkappaB) View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

bp(GO:"neuron differentiation") association p(FPLX:NFkappaB) View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

bp(GO:"protein kinase B signaling") increases act(p(FPLX:NFkappaB)) View Subject | View Object

NF-κB is a ubiquitous transcriptional factor, which can be activated by AKT pathway. PubMed:27288790

Appears in Networks:

bp(GO:"regulation of synaptic plasticity") association p(FPLX:NFkappaB) View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

bp(MESH:"Neuronal Outgrowth") association p(FPLX:NFkappaB) View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

complex(a(CHEBI:pentosidine), p(HGNC:AGER)) increases act(p(FPLX:NFkappaB)) View Subject | View Object

Two AGEs, such as pentosidine and glyceraldehyde derived pyridinium (GLAP), both found increased in AD brains, were able to upregulate BACE1 through their binding with RAGE and consequent activation of NF-κB, providing a pathologic link between diabetes and AD [49]. PubMed:27288790

Appears in Networks:

complex(a(HBP:GLAP), p(HGNC:AGER)) increases act(p(FPLX:NFkappaB)) View Subject | View Object

Two AGEs, such as pentosidine and glyceraldehyde derived pyridinium (GLAP), both found increased in AD brains, were able to upregulate BACE1 through their binding with RAGE and consequent activation of NF-κB, providing a pathologic link between diabetes and AD [49]. PubMed:27288790

Appears in Networks:

act(p(FPLX:NFkappaB)) increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

Under different envi- ronmental conditions such as Aβ/ROS/cytokines accumulation, the IκB kinase (IKK) complex becomes activated and mediates the phosphoryla- tion of IκBs, then IκBs are degradated and the remaining NF-κB dimer is activated and thus translocates to the nucleus where it binds to the DNA consensus sequence of various target genes [9–11]. PubMed:27288790

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p(FPLX:ERK) increases act(p(FPLX:NFkappaB)) View Subject | View Object

Pharmacologic inhibition of ERK and p38 MAPK and dominant- negative mutation of both enzymes suppressed Aβ-induced NF-κB transactivation thus neurotoxicity by Aβ [45,46]. PubMed:27288790

Appears in Networks:

deg(p(FPLX:IKB)) increases act(p(FPLX:NFkappaB)) View Subject | View Object

Under different envi- ronmental conditions such as Aβ/ROS/cytokines accumulation, the IκB kinase (IKK) complex becomes activated and mediates the phosphoryla- tion of IκBs, then IκBs are degradated and the remaining NF-κB dimer is activated and thus translocates to the nucleus where it binds to the DNA consensus sequence of various target genes [9–11]. PubMed:27288790

Appears in Networks:

p(FPLX:IKB, pmod(Ph)) increases act(p(FPLX:NFkappaB)) View Subject | View Object

Then the stimulation of RAGE is able to activate the mitogen-activated protein kinase signaling cascades which converge in IκB kinase complex to phosphorylate IκB, thereby release and activate NF-κB, thus trigger NF-κB dependent gene transcription including IL-1β and TNF-α, which in turn induce the translocation of NF-κB to the nucleus [50]. PubMed:27288790

Appears in Networks:

p(HGNC:IL18) increases act(p(FPLX:NFkappaB)) View Subject | View Object

Cortical neurons stimulated with IL-18 also generated NF-κB activation [33]. PubMed:27288790

Appears in Networks:
Annotations
Cell Ontology (CL)
cerebral cortex neuron

p(HGNC:IL1B) increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) 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:IL1B) increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

Then the stimulation of RAGE is able to activate the mitogen-activated protein kinase signaling cascades which converge in IκB kinase complex to phosphorylate IκB, thereby release and activate NF-κB, thus trigger NF-κB dependent gene transcription including IL-1β and TNF-α, which in turn induce the translocation of NF-κB to the nucleus [50]. PubMed:27288790

Appears in Networks:

p(HGNC:MAPK14) increases act(p(FPLX:NFkappaB)) View Subject | View Object

Pharmacologic inhibition of ERK and p38 MAPK and dominant- negative mutation of both enzymes suppressed Aβ-induced NF-κB transactivation thus neurotoxicity by Aβ [45,46]. PubMed:27288790

Appears in Networks:

p(HGNC:NFKBIA) decreases act(p(FPLX:NFkappaB)) View Subject | View Object

ROS generation leads to phosphorylation of NF-κB cytoplasmic inhibitor IκBα. NF-κB is thus liberated and transports to the nucleus. PubMed:27288790

Appears in Networks:

p(HGNC:NFKBIA, pmod(Ph)) increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

ROS generation leads to phosphorylation of NF-κB cytoplasmic inhibitor IκBα. NF-κB is thus liberated and transports to the nucleus. PubMed:27288790

Appears in Networks:

p(HGNC:TNF) increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) 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 tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

Then the stimulation of RAGE is able to activate the mitogen-activated protein kinase signaling cascades which converge in IκB kinase complex to phosphorylate IκB, thereby release and activate NF-κB, thus trigger NF-κB dependent gene transcription including IL-1β and TNF-α, which in turn induce the translocation of NF-κB to the nucleus [50]. PubMed:27288790

Appears in Networks:

p(HGNC:TNF) increases act(p(FPLX:NFkappaB)) View Subject | View Object

NSAIDs inhibit BACE1 tran- scriptional activation induced by strong NF-κB activator TNF-α. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

path(MESH:"Alzheimer Disease") positiveCorrelation act(p(FPLX:NFkappaB)) View Subject | View Object

NF-κB activation has also been detected in the brains of AD pa- tients. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Brain

path(MESH:Inflammation) association p(FPLX:NFkappaB) View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

Out-Edges 37

p(FPLX:NFkappaB) hasVariant p(FPLX:NFkappaB, pmod(Ph, Ser, 536)) View Subject | View Object

Appears in Networks:

p(FPLX:NFkappaB) hasVariant p(FPLX:NFkappaB, pmod(Ac, Lys, 122)) View Subject | View Object

Appears in Networks:

p(FPLX:NFkappaB) increases complex(g(MIRBASE:"rno-mir-195"), p(FPLX:NFkappaB)) View Subject | View Object

Chronic Brain hypoperfusion (CBH) elevates nuclear factor-kB (NF-kB), which binds with the promoter sequences of miR-195 and negatively regulates its expression. Down-regulated miR-195 up-regulates APP and BACE1 and increases Aß levels. Some Aß then enter the intracellular space and activate calpain, promoting the conversion of Cdk5/p35 to Cdk5/p25 and catalyzes the degradation of IkB (inhibitor of NF-?B)and directly phosphorylates Tau. Down-regulated miR-195 up-regulates p35, which provides the active substrates of p25 PubMed:26118667

Appears in Networks:

p(FPLX:NFkappaB) association a(PUBCHEM:5318517) View Subject | View Object

Tab. 1A-B: Summary of the Tau aggregation modulators (inhibitors = 18 (A), stimulators = 10 (B)) which show decrease / increase in the amount of ThS + cells without affecting the expression level of TauRD∆K compared to the compound untreated control. PubMed:30640040

Appears in Networks:

act(p(FPLX:NFkappaB), ma(tscript)) increases r(HGNC:BACE1) View Subject | View Object

Our data clearly demonstrate that NSAIDs inhibit TNF-a-induced BACE1 transcription via its NF-kB cis-acting elements. PubMed:21329555

Appears in Networks:

p(FPLX:NFkappaB) hasVariant p(FPLX:NFkappaB, pmod(Ph)) View Subject | View Object

Appears in Networks:

act(p(FPLX:NFkappaB)) association bp(GO:"inflammatory response") View Subject | View Object

Furthermore, A induced NF-B activity in glial and neuronal cells. NF-B is involved in inflammatory responses and is expressed in brains of AD patients [32]. PubMed:29179999

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

tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) increases bp(GO:"inflammatory response") View Subject | View Object

ROS activate various downstream signaling molecules, such as PKC and mitogen-activated protein kinases (MAPKs) that induce nuclear translocation of NF-B and the expression of pro-inflammatory genes [41]. PubMed:29179999

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p(FPLX:NFkappaB) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Furthermore, A induced NF-B activity in glial and neuronal cells. NF-B is involved in inflammatory responses and is expressed in brains of AD patients [32]. PubMed:29179999

Appears in Networks:
Annotations
MeSH
Brain

act(p(FPLX:NFkappaB)) association path(HP:Neurodegeneration) View Subject | View Object

Degeneration of neurons in the brain of AD patients is associated with the activation of NF-B [7 PubMed:29179999

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(p(FPLX:NFkappaB)) regulates p(FPLX:"NADPH_oxidase") View Subject | View Object

NF-B activation mediates the expression of the pro-oxidant NAPDH oxidase, cyclooxygenase 2 (COX2), interleukins and the antioxidant enzyme, superoxide dismutase (SOD) [78]. Additionally, NF-B activity is associated with the expression of BACE1 [79] and the activation of nucleotide-binding oligomerization domain-like receptor (NALP) 3 inflammosome [80]. PubMed:29179999

Appears in Networks:

act(p(FPLX:NFkappaB)) regulates p(HGNC:PTGS2) View Subject | View Object

NF-B activation mediates the expression of the pro-oxidant NAPDH oxidase, cyclooxygenase 2 (COX2), interleukins and the antioxidant enzyme, superoxide dismutase (SOD) [78]. Additionally, NF-B activity is associated with the expression of BACE1 [79] and the activation of nucleotide-binding oligomerization domain-like receptor (NALP) 3 inflammosome [80]. PubMed:29179999

Appears in Networks:

act(p(FPLX:NFkappaB)) regulates a(MESH:Interleukins) View Subject | View Object

NF-B activation mediates the expression of the pro-oxidant NAPDH oxidase, cyclooxygenase 2 (COX2), interleukins and the antioxidant enzyme, superoxide dismutase (SOD) [78]. Additionally, NF-B activity is associated with the expression of BACE1 [79] and the activation of nucleotide-binding oligomerization domain-like receptor (NALP) 3 inflammosome [80]. PubMed:29179999

Appears in Networks:

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

NF-B activation mediates the expression of the pro-oxidant NAPDH oxidase, cyclooxygenase 2 (COX2), interleukins and the antioxidant enzyme, superoxide dismutase (SOD) [78]. Additionally, NF-B activity is associated with the expression of BACE1 [79] and the activation of nucleotide-binding oligomerization domain-like receptor (NALP) 3 inflammosome [80]. PubMed:29179999

Appears in Networks:

act(p(FPLX:NFkappaB)) increases p(HGNC:BACE1) View Subject | View Object

NF-B activation mediates the expression of the pro-oxidant NAPDH oxidase, cyclooxygenase 2 (COX2), interleukins and the antioxidant enzyme, superoxide dismutase (SOD) [78]. Additionally, NF-B activity is associated with the expression of BACE1 [79] and the activation of nucleotide-binding oligomerization domain-like receptor (NALP) 3 inflammosome [80]. PubMed:29179999

Appears in Networks:

p(FPLX:NFkappaB) association path(MESH:Inflammation) View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

p(FPLX:NFkappaB) association bp(GO:"negative regulation of neuron apoptotic process") View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

p(FPLX:NFkappaB) association bp(GO:"neuron differentiation") View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

p(FPLX:NFkappaB) association bp(GO:"apoptotic process") View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

p(FPLX:NFkappaB) association bp(MESH:"Neuronal Outgrowth") View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

p(FPLX:NFkappaB) association bp(GO:"regulation of synaptic plasticity") View Subject | View Object

In the nervous system, NF-κB has been proposed to serve important function by acting as a transcription regulator: it has roles in inflammation, neuronal survival, differentiation, apoptosis, neurite outgrowth, and synaptic plasticity [5], which are impaired in the progression of various neurodegenerative diseases especially in AD. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Nervous System

act(p(FPLX:NFkappaB)) increases tloc(p(FPLX:NFkappaB), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

Under different envi- ronmental conditions such as Aβ/ROS/cytokines accumulation, the IκB kinase (IKK) complex becomes activated and mediates the phosphoryla- tion of IκBs, then IκBs are degradated and the remaining NF-κB dimer is activated and thus translocates to the nucleus where it binds to the DNA consensus sequence of various target genes [9–11]. PubMed:27288790

Appears in Networks:

act(p(FPLX:NFkappaB)) increases complex(a(MESH:DNA), p(FPLX:NFkappaB)) View Subject | View Object

Under different envi- ronmental conditions such as Aβ/ROS/cytokines accumulation, the IκB kinase (IKK) complex becomes activated and mediates the phosphoryla- tion of IκBs, then IκBs are degradated and the remaining NF-κB dimer is activated and thus translocates to the nucleus where it binds to the DNA consensus sequence of various target genes [9–11]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cell Nucleus

act(p(FPLX:NFkappaB)) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

NF-κB activation has also been detected in the brains of AD pa- tients. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Brain

act(p(FPLX:NFkappaB)) increases p(HGNC:IL1B) View Subject | View Object

Then the stimulation of RAGE is able to activate the mitogen-activated protein kinase signaling cascades which converge in IκB kinase complex to phosphorylate IκB, thereby release and activate NF-κB, thus trigger NF-κB dependent gene transcription including IL-1β and TNF-α, which in turn induce the translocation of NF-κB to the nucleus [50]. PubMed:27288790

Appears in Networks:

act(p(FPLX:NFkappaB)) increases p(HGNC:TNF) View Subject | View Object

Then the stimulation of RAGE is able to activate the mitogen-activated protein kinase signaling cascades which converge in IκB kinase complex to phosphorylate IκB, thereby release and activate NF-κB, thus trigger NF-κB dependent gene transcription including IL-1β and TNF-α, which in turn induce the translocation of NF-κB to the nucleus [50]. PubMed:27288790

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act(p(FPLX:NFkappaB)) decreases p(HGNC:UCHL1) View Subject | View Object

The decrease in Uch-L1 depends on NF-κB pathway since NF-κB p65 can interact with the −300 bp and −109 bp NF-κB binding sequences of the Uch-L1 gene promoter [55]. PubMed:27288790

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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

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p(FPLX:NFkappaB) regulates bp(GO:"inflammatory response") View Subject | View Object

Inflammation is a key pathological hall mark of AD [61,62], NF-κB is considered as a primary regulator of inflammatory processes [10]. PubMed:27288790

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act(p(FPLX:NFkappaB)) increases a(MESH:Cytokines) View Subject | View Object

Inhibition of NF-κB leads to decreased induction of cytokines and chemokines by IL-1β and TNF-α. PubMed:27288790

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act(p(FPLX:NFkappaB)) increases a(MESH:Chemokines) View Subject | View Object

Inhibition of NF-κB leads to decreased induction of cytokines and chemokines by IL-1β and TNF-α. PubMed:27288790

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p(FPLX:NFkappaB) regulates p(HGNC:PTGS2) View Subject | View Object

In addition, COX-2, mainly regulated by NF-κB, is notably upregulated in the brains of AD patients, which may be associated with the formation of Aβ plaque [65]. PubMed:27288790

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p(FPLX:NFkappaB) increases m(MIRBASE:"hsa-mir-125b-1") View Subject | View Object

Inducible miRNAs and lncRNA perform critical regulatory roles in CNS development, several brain-enriched miRNAs are consistently up- regulated by NF-κB, including miRNA-125b [66], miRNA-146a [67] and miRNA-155 [68]. PubMed:27288790

Appears in Networks:

p(FPLX:NFkappaB) increases m(MIRBASE:"hsa-mir-125b-2") View Subject | View Object

Inducible miRNAs and lncRNA perform critical regulatory roles in CNS development, several brain-enriched miRNAs are consistently up- regulated by NF-κB, including miRNA-125b [66], miRNA-146a [67] and miRNA-155 [68]. PubMed:27288790

Appears in Networks:

p(FPLX:NFkappaB) increases m(MIRBASE:"hsa-mir-146a") View Subject | View Object

Inducible miRNAs and lncRNA perform critical regulatory roles in CNS development, several brain-enriched miRNAs are consistently up- regulated by NF-κB, including miRNA-125b [66], miRNA-146a [67] and miRNA-155 [68]. PubMed:27288790

Appears in Networks:

p(FPLX:NFkappaB) increases m(MIRBASE:"hsa-mir-155") View Subject | View Object

Inducible miRNAs and lncRNA perform critical regulatory roles in CNS development, several brain-enriched miRNAs are consistently up- regulated by NF-κB, including miRNA-125b [66], miRNA-146a [67] and miRNA-155 [68]. PubMed:27288790

Appears in Networks:

act(p(FPLX:NFkappaB), ma(tscript)) increases m(MIRBASE:"hsa-mir-155") View Subject | View Object

Moreover, miRNA-155 is strongly and rapidly up-regulated by inflammatory cytokines and also is an inducible miRNA under transcriptional control by NF-κB. 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.