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p(HGNC:NFKB1)

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Entity

Name
NFKB1
Namespace
hgnc
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

Appears in Networks 6

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

Activation and regulation of the inflammasomes v1.0.0

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis 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

Heme Curation v0.0.1-dev

Mechanistic knowledge surrounding heme

In-Edges 15

a(GO:"neurofibrillary tangle") increases p(HGNC:NFKB1) 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

bp(GO:"long-term synaptic potentiation") decreases p(HGNC:NFKB1) View Subject | View Object

The expression of p65 and p50 is induced in response to long-term changes in synaptic strength and transmission such as LTP [39] and LTD PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

bp(GO:"long-term synaptic depression") decreases p(HGNC:NFKB1) View Subject | View Object

The expression of p65 and p50 is induced in response to long-term changes in synaptic strength and transmission such as LTP [39] and LTD PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(p(HGNC:BACE1), p(HGNC:NFKB1), p(HGNC:RELA)) hasComponent p(HGNC:NFKB1) View Subject | View Object

Appears in Networks:

complex(p(HGNC:NFKB1), p(HGNC:RELA)) hasComponent p(HGNC:NFKB1) View Subject | View Object

Appears in Networks:

complex(p(HGNC:NFKB1), p(HGNC:RELA), p(HGNC:SYP)) hasComponent p(HGNC:NFKB1) View Subject | View Object

Appears in Networks:

a(CHEBI:"amyloid-beta") increases act(p(HGNC:NFKB1)) View Subject | View Object

Further investigations confirm that the activation of p50 and RelA subunit contributes to the apoptotic program in cells exposed to the Aβ [17]. PubMed:27288790

Appears in Networks:

complex(a(GO:"NF-kappaB complex"), p(HGNC:NFKB1), p(HGNC:RELA)) hasComponent p(HGNC:NFKB1) View Subject | View Object

Appears in Networks:

a(CHEBI:heme) increases p(HGNC:NFKB1) View Subject | View Object

Cell-free hemoglobin and its prosthetic group heme can contribute to organ dysfunction and death [1–4, 9–12]; the pathological mechanisms include nitric oxide consumption, vasoconstriction, oxidative injury to lipid membranes, activation of the transcription factor NF-κB, endothelial injury as well as iron-driven oxidative inhibition of glucose metabolism[10–14]. PubMed:29956069

Appears in Networks:
Annotations
Text Location
Review

a(CHEBI:heme) increases p(HGNC:NFKB1) View Subject | View Object

Heme/TLR-4 signaling, moreover, was found to activate NF-κB and trigger vaso-occlusion [42]. PubMed:29956069

Appears in Networks:
Annotations
MeSH
Arteries
MeSH
Sepsis
Text Location
Review

p(HGNC:TLR4) increases p(HGNC:NFKB1) View Subject | View Object

TLR4 activation leads to MAPKs and NFκB activation, which are necessary to TNF secretion. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

act(p(HGNC:IRF3)) increases p(HGNC:NFKB1) View Subject | View Object

The MyD88-dependent pathway leads to the activation of mitogen-activated protein kinases (MAPKs) and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) transcription factors inducing the expression of inflammatory cytokines such as TNF, IL-6, IL-1β, and KC (Takeuchi and Akira, 2010) PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

p(HGNC:MYD88) increases act(p(HGNC:NFKB1)) View Subject | View Object

Moreover, human embryonic kidney (HEK) cells transfected with human TLR4 secretes IL-8 upon stimulation with heme (Piazza et al., 2011). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

p(HGNC:MYD88) increases act(p(HGNC:NFKB1)) View Subject | View Object

Only under protein-free conditions did we observe a limited heme-induced TNF-alpha response in cultured macrophages, which was triggered via signaling of the classical TLR4–MyD88–TRIF pathway of NF-kB activation.28 PubMed:29610666

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Mitochondria
Text Location
Discussion

p(HGNC:TICAM1) increases act(p(HGNC:NFKB1)) View Subject | View Object

Only under protein-free conditions did we observe a limited heme-induced TNF-alpha response in cultured macrophages, which was triggered via signaling of the classical TLR4–MyD88–TRIF pathway of NF-kB activation.28 PubMed:29610666

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Mitochondria
Text Location
Discussion

Out-Edges 10

p(HGNC:NFKB1) increases p(HGNC:IL1B) View Subject | View Object

The transcription of pro-IL-1β is induced by the activation of the transcription factor nuclear factor-κB (NF-κB), whereas pro-IL-18 is constitutively expressed and its expression is increased after cellular activation. PubMed:23702978

Appears in Networks:
Annotations
Confidence
High
NeuroMMSigDB
Interleukin signaling subgraph
NeuroMMSigDB
Nuclear factor Kappa beta subgraph

p(HGNC:NFKB1) increases path(MESH:"Spatial Memory") View Subject | View Object

p50 knock-out mice exhibit deficits in late LTP resulting in compromised spatial memory PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:NFKB1) increases bp(GO:"long-term synaptic potentiation") View Subject | View Object

p50 knock-out mice exhibit deficits in late LTP resulting in compromised spatial memory PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:NFKB1) increases bp(GO:learning) View Subject | View Object

p50 knock-out mice exhibit severe deficits in learning as assessed by an active avoidance assay [93] in addition to displaying lack of anxiety-like behavior in well-established tests and paradigms that assess exploratory drive as a measure of anxiety PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:NFKB1) increases path(MESH:Anxiety) View Subject | View Object

p50 knock-out mice exhibit severe deficits in learning as assessed by an active avoidance assay [93] in addition to displaying lack of anxiety-like behavior in well-established tests and paradigms that assess exploratory drive as a measure of anxiety PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(p(HGNC:NFKB1)) increases bp(GO:"apoptotic process") View Subject | View Object

Further investigations confirm that the activation of p50 and RelA subunit contributes to the apoptotic program in cells exposed to the Aβ [17]. PubMed:27288790

Appears in Networks:

p(HGNC:NFKB1) increases p(HGNC:TNF) View Subject | View Object

TLR4 activation leads to MAPKs and NFκB activation, which are necessary to TNF secretion. PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

act(p(HGNC:NFKB1)) increases p(HGNC:TNF) View Subject | View Object

Only under protein-free conditions did we observe a limited heme-induced TNF-alpha response in cultured macrophages, which was triggered via signaling of the classical TLR4–MyD88–TRIF pathway of NF-kB activation.28 PubMed:29610666

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Mitochondria
Text Location
Discussion

p(HGNC:NFKB1) increases p(HGNC:CXCL8) View Subject | View Object

Moreover, human embryonic kidney (HEK) cells transfected with human TLR4 secretes IL-8 upon stimulation with heme (Piazza et al., 2011). PubMed:24904418

Appears in Networks:
Annotations
Cell Ontology (CL)
leukocyte
MeSH
Liver
MeSH
Malaria
Text Location
Review

p(HGNC:NFKB1) increases a(MESH:Cytokines) View Subject | View Object

Furthermore, cytokine secretion depends on the coordinated iron in the porphyrin ring (Figueiredo et al, 2007), and nuclear factor-jB (NF-jB), MAPKs activation and ROS are essential for the increase in cytokine production induced by haem (Fernandez et al, 2010). PubMed:25307023

Appears in Networks:
Annotations
Cell Ontology (CL)
macrophage
MeSH
Plasma
MeSH
Urine
MeSH
Anemia, Hemolytic, Autoimmune
Text Location
Review

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.