1. Catalog
  2. Nodes
  3. r(HGNC:BACE1)

r(HGNC:BACE1)

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
BACE1
Namespace
HGNC
Namespace Version
20180215
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/namespace/hgnc/hgnc-20180215.belns

Appears in Networks 7

APP processing in Alzheimer's disease v1.0.1

APP processing in Alzheimer's disease

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

The Spleen Tyrosine Kinase (Syk) Regulates Alzheimer Amyloid-β Production and Tau Hyperphosphorylation* v1.0.0

New insights into the role of microRNAs and long noncoding RNAs in most common neurodegenerative diseases v1.0.0

Increased NF-κB signalling up-regulates BACE1 expression and its therapeutic potential in Alzheimer's disease. v1.0.0

Upstream regulators and downstream effectors of NF-κBinAlzheimer's disease v1.0.0

In-Edges 33

a(CHEBI:testosterone) decreases r(HGNC:BACE1) View Subject | View Object

However, a recent study blocking the conversion of testosterone to estrogen found an estrogen-independent improvement in cognitive function and lowering of plaque formation along with a decrease in BACE1 mRNA, protein level, and activity [211]. In addition, testosterone may also reduce the protein level of PS1 [196] PubMed:21214928

Appears in Networks:
Annotations
MeSH
Cell Membrane
Confidence
Medium
MeSH
Hippocampus
MeSH
Down Syndrome

a(CHEBI:Anatabine) decreases r(HGNC:BACE1) View Subject | View Object

As expected, TNFα greatly stimulated BACE-1 transcription whereas anatabine fully prevented the increase in BACE-1 mRNA levels induced by TNFα (Fig. 7A). PubMed:21958873

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

a(CHEBI:"amyloid-beta") increases r(HGNC:BACE1) View Subject | View Object

Additionally, we found that Bace1 mRNA expression is significantly increased in the brain of Tg PS1/APPswe mice compared to wild- type littermates, whereas a significant reduction in Bace1 mRNA levels is observed in Tg PS1/ APPswe receiving 20 mg/Kg/Day of anatabine in their drinking water showing that at this dosage anatabine can mitigate the upregulation of Bace1 expression in Tg PS1/APPswe mice (Fig 9). PubMed:26010758

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Alzheimer Disease

a(CHEBI:Anatabine) decreases r(HGNC:BACE1) View Subject | View Object

Additionally, we found that Bace1 mRNA expression is significantly increased in the brain of Tg PS1/APPswe mice compared to wild- type littermates, whereas a significant reduction in Bace1 mRNA levels is observed in Tg PS1/ APPswe receiving 20 mg/Kg/Day of anatabine in their drinking water showing that at this dosage anatabine can mitigate the upregulation of Bace1 expression in Tg PS1/APPswe mice (Fig 9). PubMed:26010758

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Alzheimer Disease

a(CHEBI:"2-[[7-(3,4-dimethoxyphenyl)-5-imidazo[1,2-c]pyrimidinyl]amino]-3-pyridinecarboxamide") decreases r(HGNC:BACE1) View Subject | View Object

We found that, like (-)-nilvadipine, Syk inhibition with the selective Syk inhibitor BAY61-3606 resulted in decreased sAPPβ secretion, BACE-1 mRNA, and BACE-1 protein expression (data not shown). PubMed:25331948

Appears in Networks:

a(CHEBI:Nilvadipine) decreases r(HGNC:BACE1) View Subject | View Object

We found that both (-)-nilvadipine and racemic nilvadipine reduce BACE-1 mRNA expression (Fig. 1C) induced by TNFα PubMed:25331948

Appears in Networks:

a(CHEBI:Nilvadipine) decreases r(HGNC:BACE1) View Subject | View Object

We found that, like (-)-nilvadipine, Syk inhibition with the selective Syk inhibitor BAY61-3606 resulted in decreased sAPPβ secretion, BACE-1 mRNA, and BACE-1 protein expression (data not shown). PubMed:25331948

Appears in Networks:

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

We found that, like (-)-nilvadipine, Syk inhibition with the selective Syk inhibitor BAY61-3606 resulted in decreased sAPPβ secretion, BACE-1 mRNA, and BACE-1 protein expression (data not shown). PubMed:25331948

Appears in Networks:

complex(g(HGNC:"MIR124-1"), r(HGNC:BACE1)) hasComponent r(HGNC:BACE1) View Subject | View Object

Appears in Networks:

complex(g(HGNC:"MIR124-1"), r(HGNC:BACE1)) decreases act(r(HGNC:BACE1)) View Subject | View Object

It is interesting to note that miR‐124 has a target sequence on BACE1 mRNA, and by binding to it, it inhibits mRNA. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(g(HGNC:"MIR153-1"), r(HGNC:BACE1)) hasComponent r(HGNC:BACE1) View Subject | View Object

Appears in Networks:

complex(g(HGNC:MIR15B), r(HGNC:BACE1)) hasComponent r(HGNC:BACE1) View Subject | View Object

Appears in Networks:

complex(g(HGNC:MIR186), r(HGNC:BACE1)) hasComponent r(HGNC:BACE1) View Subject | View Object

Appears in Networks:

complex(g(HGNC:MIR339), r(HGNC:BACE1)) hasComponent r(HGNC:BACE1) View Subject | View Object

Appears in Networks:

complex(g(HGNC:MIR384), r(HGNC:BACE1)) hasComponent r(HGNC:BACE1) View Subject | View Object

Appears in Networks:

path(MESH:"Alzheimer Disease") positiveCorrelation r(HGNC:BACE1, loc(GO:cytoplasm)) View Subject | View Object

For instance, measuring lncRNA BACE1 within the cytoplasm of the patients showed that its level in patients with Alzheimer’s was significantly higher than that in the control group PubMed:30663117

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

r(HGNC:"BACE1-AS") increases r(HGNC:BACE1) View Subject | View Object

BACE1‐AS can increase the expression of BACE1 mRNA by increasing its stability, which gives rise to AD PubMed:30663117

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:"acetylsalicylic acid") decreases r(HGNC:BACE1) View Subject | View Object

Compared to controls, TNF-a treatment resulted in significant increase in luciferase activity in the cells transfected with the human BACE1 promoter pB1P- N1 plasmid (p<0.005) and addition of aspirin in- hibited the BACE1 transcriptional activation induced by TNF-a (p<0.005 relative to TNF-a and p>0.05 relative to controls) (Fig. 6a). PubMed:21329555

Appears in Networks:

a(CHEBI:"acetylsalicylic acid") decreases r(HGNC:BACE1) View Subject | View Object

Consistent with pB1P-N1 plasmid results, TNF-a significantly induced BACE1-NF-kB promoter activation (p<0.005) and the NSAIDs aspirin, ibuprofen and indomethacin significantly blocked the TNF-a-induced BACE1- NF-kB promoter activation (p<0.005) (Fig. 6b). PubMed:21329555

Appears in Networks:

a(CHEBI:ibuprofen) decreases r(HGNC:BACE1) View Subject | View Object

Consistent with pB1P-N1 plasmid results, TNF-a significantly induced BACE1-NF-kB promoter activation (p<0.005) and the NSAIDs aspirin, ibuprofen and indomethacin significantly blocked the TNF-a-induced BACE1- NF-kB promoter activation (p<0.005) (Fig. 6b). PubMed:21329555

Appears in Networks:

a(MESH:"Anti-Inflammatory Agents, Non-Steroidal") decreases 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:

a(PUBCHEM:3715) decreases r(HGNC:BACE1) View Subject | View Object

Consistent with pB1P-N1 plasmid results, TNF-a significantly induced BACE1-NF-kB promoter activation (p<0.005) and the NSAIDs aspirin, ibuprofen and indomethacin significantly blocked the TNF-a-induced BACE1- NF-kB promoter activation (p<0.005) (Fig. 6b). PubMed:21329555

Appears in Networks:

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

These results suggest that the 4NF-kB oligonucleotides con- taining four putative NF-kB-binding elements from the human BACE1 promoter is able to respond to NF-kB signalling to modulate a downstream gene transcription. PubMed:21329555

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:

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

Consistent with our Western blot results, a significant elevation of promoter activity was detected in cells co- expressing BACE1 reporter plasmid and NF-kB p65 (Fig. 3d). PubMed:21329555

Appears in Networks:

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:TNF) increases r(HGNC:BACE1) View Subject | View Object

Compared to controls, TNF-a treatment resulted in significant increase in luciferase activity in the cells transfected with the human BACE1 promoter pB1P- N1 plasmid (p<0.005) and addition of aspirin in- hibited the BACE1 transcriptional activation induced by TNF-a (p<0.005 relative to TNF-a and p>0.05 relative to controls) (Fig. 6a). PubMed:21329555

Appears in Networks:

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

Consistent with pB1P-N1 plasmid results, TNF-a significantly induced BACE1-NF-kB promoter activation (p<0.005) and the NSAIDs aspirin, ibuprofen and indomethacin significantly blocked the TNF-a-induced BACE1- NF-kB promoter activation (p<0.005) (Fig. 6b). PubMed:21329555

Appears in Networks:

a(CHEBI:ibuprofen) decreases r(HGNC:BACE1) View Subject | View Object

Further- more, naproxen and ibuprofen and perhaps other NSAIDs, can block the inflammation-induced BACE1 transcription and Aβ production [52,87]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

a(CHEBI:naproxen) decreases r(HGNC:BACE1) View Subject | View Object

Further- more, naproxen and ibuprofen and perhaps other NSAIDs, can block the inflammation-induced BACE1 transcription and Aβ production [52,87]. PubMed:27288790

Appears in Networks:
Annotations
MeSH
Cerebral Cortex
MeSH
Hippocampus

composite(p(HGNC:GSK3B), p(HGNC:RELA)) increases r(HGNC:BACE1) View Subject | View Object

Disruption of NF-κB p65 expression in RelA-KO cells abolished GSK3β's effect on the transcriptional activation of the human BACE1 gene promoter. PubMed:27288790

Appears in Networks:

r(HGNC:"BACE1-AS") regulates r(HGNC:BACE1) View Subject | View Object

BACE1-AS regulates BACE1 mRNA and subsequently BACE1 protein expression in vitro and in vivo. PubMed:27288790

Appears in Networks:

r(HGNC:"BACE1-AS") decreases deg(r(HGNC:BACE1)) View Subject | View Object

Upon exposure to various cell stressors including Aβ 42 , expression of BACE1-AS becomes elevated, increasing BACE1 mRNA stability and generating additional Aβ 42 through a post-transcriptional feed-forward mechanism [74]. PubMed:27288790

Appears in Networks:

Out-Edges 2

r(HGNC:BACE1, loc(GO:cytoplasm)) positiveCorrelation path(MESH:"Alzheimer Disease") View Subject | View Object

For instance, measuring lncRNA BACE1 within the cytoplasm of the patients showed that its level in patients with Alzheimer’s was significantly higher than that in the control group PubMed:30663117

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

r(HGNC:BACE1) increases path(MESH:"Alzheimer Disease") View Subject | View Object

BACE1‐AS can increase the expression of BACE1 mRNA by increasing its stability, which gives rise to AD PubMed:30663117

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.