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p(HGNC:RELA)

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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 8

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

RelB/p50 complexes regulate cytokine-induced YKL-40 expression v1.0.0

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

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 23

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

Appears in Networks:

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:RELA) View Subject | View Object

The results showed that the protein level of p65 sig- nificantly increased to 155.40¡13.39% in AD patient samples relative to control samples (p<0.05) (Fig. 1a). PubMed:21329555

Appears in Networks:
Annotations
MeSH
Prefrontal Cortex

bp(GO:"apoptotic process") negativeCorrelation p(HGNC:RELA) View Subject | View Object

Overexpression of the p65 subunit of NF-κB confers resistance to etoposide-induced apoptosis in cortical neurons PubMed:28745240

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

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

Appears in Networks:

complex(p(HGNC:BACE1), p(HGNC:NFKB2), p(HGNC:RELA)) hasComponent p(HGNC:RELA) View Subject | View Object

Appears in Networks:

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

Appears in Networks:

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

Appears in Networks:

complex(p(HGNC:NFKB2), p(HGNC:RELA)) hasComponent p(HGNC:RELA) View Subject | View Object

Appears in Networks:

a(CHEBI:Salidroside) regulates p(HGNC:RELA) View Subject | View Object

Salidroside ameliorated cognitive injury in an AD rat model by regulating the expressions of thioredoxin, thioredoxin interacting protein and NF-B pathway proteins such as NF-B p65, IB, IKK and IKK[137]. PubMed:29179999

Appears in Networks:

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

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

Appears in Networks:

a(CHEBI:curcumin) decreases tloc(p(HGNC:RELA), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) 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(PUBCHEM:164676) decreases act(p(HGNC:RELA)) 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:73078) decreases tloc(p(HGNC:RELA), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) 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:

a(CHEBI:"amyloid-beta") increases act(p(HGNC:RELA)) 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:

composite(p(HGNC:GSK3B), p(HGNC:RELA)) hasComponent p(HGNC:RELA) View Subject | View Object

Appears in Networks:

act(p(FPLX:AKT)) increases p(HGNC:RELA) View Subject | View Object

Activation of AKT augments the transactivating activity and produces higher nuclear levels of p65-NF- κB, which is important for neuroprotection. PubMed:27288790

Appears in Networks:

p(FPLX:NFkappaB, pmod(Ph, Ser, 536)) increases act(p(HGNC:RELA)) View Subject | View Object

Results have shown a sig- nificant increase in phosphorylation of IκB at serine 32–36 and NF-κB at serine 536 with Aβ 42 exposure, this phosphorylation enhances p65 transactivation potential [16]. PubMed:27288790

Appears in Networks:

act(p(HGNC:MAPK14)) increases tloc(p(HGNC:RELA), fromLoc(MESH:Cytosol), toLoc(MESH:"Cell Nucleus")) View Subject | View Object

Treatment with p38 inhibitor, SB239063, prevents downstream phosphorylation of IκBα and p65 translocation to the nucleus in the ventral midbrain. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Mesencephalon

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

Appears in Networks:

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

Appears in Networks:

path(MESH:"Alzheimer Disease") positiveCorrelation p(HGNC:RELA) View Subject | View Object

Comparison of the cellular distribution of NF-κB in the nucleus basalis of Meynert of AD and control patients showed that the proportion of large cholinergic neurons with elevated nuclear p65 was significantly increased in AD, suggesting an association between NF–κB functions and the process of cholinergic degeneration PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

Out-Edges 16

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

Appears in Networks:

p(HGNC:RELA) causesNoChange p(HGNC:CHI3L1) View Subject | View Object

In these cells, basal expression of YKL-40 is RelB-, p65-, and STAT3-independent, implicating other unknown factors. PubMed:25681350

Appears in Networks:
Annotations
Cell Ontology (CL)
chondrocyte

p(HGNC:RELA) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

The results showed that the protein level of p65 sig- nificantly increased to 155.40¡13.39% in AD patient samples relative to control samples (p<0.05) (Fig. 1a). PubMed:21329555

Appears in Networks:
Annotations
MeSH
Prefrontal Cortex

p(HGNC:RELA) increases r(HGNC:BACE1) View Subject | View Object

When wild-type cells were transfected with NF-kB p65 expression plasmid, the mRNA level of BACE1 was elevated by 476.6¡21.68% (p<0.0001 relative to controls) (Fig. 5b). PubMed:21329555

Appears in Networks:

p(HGNC:RELA) increases p(HGNC:BACE1) View Subject | View Object

Our result showed that p65 overexpression significantly increased BACE1 protein level by 232.54¡12.86% (p<0.01 relative to controls) (Fig. 5g). PubMed:21329555

Appears in Networks:

p(HGNC:RELA) increases p(HBP:C99) View Subject | View Object

p65 expression significantly increased the amount of C99 in 20E2 cells by 152.29¡6.03% in the presence of NF-kB p65 relative to controls (p<0.001) (Fig. 5h, i). PubMed:21329555

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

p(HGNC:RELA) causesNoChange p(HGNC:APP) View Subject | View Object

There was no significant difference in APP level between p65 transfected cells and controls (p>0.05). PubMed:21329555

Appears in Networks:

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

The results showed that NF-kB p65 expression significantly increased total Ab protein concentration by 134.90¡5.74% in SAS1 cells, a stable SH-SY5Y cell stably expressing Swedish mutant APP695 (Sun et al. 2006a) (p<0.0001) (Fig. 5j). PubMed:21329555

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

p(HGNC:RELA) hasVariant p(HGNC:RELA, pmod(Ph, Ser, 536)) View Subject | View Object

Appears in Networks:

p(HGNC:RELA) increases bp(MESH:"Synaptic Transmission") View Subject | View Object

The indispensable role of NF-κB in synaptic transmission is corroborated by the fact that the mice that are deficient in neuronal p65, exhibit severe deficits in hippocampal basal synaptic transmission and long term potentiation (LTP) PubMed:28745240

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

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

The indispensable role of NF-κB in synaptic transmission is corroborated by the fact that the mice that are deficient in neuronal p65, exhibit severe deficits in hippocampal basal synaptic transmission and long term potentiation (LTP) PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:RELA) negativeCorrelation bp(GO:"apoptotic process") View Subject | View Object

Overexpression of the p65 subunit of NF-κB confers resistance to etoposide-induced apoptosis in cortical neurons PubMed:28745240

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

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

Appears in Networks:

act(p(HGNC:RELA)) 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:RELA) decreases bp(GO:"neuron apoptotic process") View Subject | View Object

Activation of AKT augments the transactivating activity and produces higher nuclear levels of p65-NF- κB, which is important for neuroprotection. PubMed:27288790

Appears in Networks:

p(HGNC:RELA) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

Comparison of the cellular distribution of NF-κB in the nucleus basalis of Meynert of AD and control patients showed that the proportion of large cholinergic neurons with elevated nuclear p65 was significantly increased in AD, suggesting an association between NF–κB functions and the process of cholinergic degeneration PubMed:25652642

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

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.