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a(CHEBI:"amyloid-beta polypeptide 40")

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Entity

Name
amyloid-beta polypeptide 40
Namespace
chebi
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/chebi-names.belns

Appears in Networks 11

A role for APP in Wnt signalling links synapse loss with β-amyloid production. v1.0.0

Effects of peptides derived from BACE1 catalytic domain on APP processing v1.0.0

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

Role of the nicotinic acetylcholine receptor in Alzheimer's disease pathology and treatment v1.0.1

Nuclear receptors as therapeutic targets for Alzheimer's disease. v1.0.0

The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0

Clearance systems in the brain-implications for Alzheimer disease. v1.0.1

Clearance of Amyloid Beta and Tau in Alzheimer’s Disease:from Mechanisms to Therapy v1.0.1

Anatabine lowers Alzheimer's Aβ production in vitro and in vivo v1.0.0

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

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

In-Edges 23

a(CHEBI:"fasudil hydrochloride") decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

Fasudil also reversed the stimulatory effect of Vangl2 and Dkk1 on Aβ production in the same cells as determined by ELISA based quantification of Aβ1–40 levels in the paired culture media from the same experiments (Fig. 3d). PubMed:30232325

Appears in Networks:
Annotations
Confidence
High

a(CHEBI:"fasudil hydrochloride") decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

Animals receiving fasudil had significantly lower soluble Aβ1–40 levels than controls (Fig. 4b). PubMed:30232325

Appears in Networks:
Annotations
Confidence
High

p(HGNC:BACE1, frag("228_236")) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

BI-1 treatment effectively reduced Ab 40 levels (IC50 = 0.06 mM) in the conditioned medium. BI-3 also inhibited Ab 40 production (IC50 = 0.2 mM), although the effective concentrations were relatively high compared to those of BI-1. PubMed:17293005

Appears in Networks:

p(HGNC:BACE1, frag("67_78")) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

BI-1 treatment effectively reduced Ab 40 levels (IC50 = 0.06 mM) in the conditioned medium. BI-3 also inhibited Ab 40 production (IC50 = 0.2 mM), although the effective concentrations were relatively high compared to those of BI-1. PubMed:17293005

Appears in Networks:

composite(a(CHEBI:"amyloid-beta polypeptide 40"), a(CHEBI:"amyloid-beta polypeptide 42")) hasComponent a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

Appears in Networks:

a(CHEBI:nicotine) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

The analysis of the Abeta fraction reduced by nicotine showed that mainly insoluble Ab1-40/42 was affected while there was no change in soluble Abeta (Nordberg et al., 2002) PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

a(CHEBI:nicotine) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

The short-term treatment of 10 days showed a significant reduction in cortical insoluble Abeta1-40/42 PubMed:25514383

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

complex(a(CHEBI:"amyloid-beta polypeptide 40"), a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) hasComponent a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

Appears in Networks:

complex(a(CHEBI:"amyloid-beta polypeptide 40"), p(MGI:Chrna7)) hasComponent a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

Appears in Networks:

p(HGNC:BACE1) increases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

The Ab peptide is generated by the sequential cleavage of the amyloid precursor protein (APP) by the b and g secretases, resulting in the generation of peptides 40 or 42 amino acids in length [2]. PubMed:21718217

Appears in Networks:
Annotations
Confidence
Medium

rxn(reactants(p(HGNC:APP)), products(a(CHEBI:"amyloid-beta polypeptide 40"), a(CHEBI:"amyloid-beta polypeptide 42"))) hasProduct a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

Appears in Networks:

path(MESH:"Alzheimer Disease") association a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

Given the size of AD-related proteins, mono- meric Aβ1-40, Aβ1-42 and tau, should be able to pass freely through astrocytic endfeet clefts at the glial barrier.72 PubMed:26195256

Appears in Networks:

a(CHEBI:calcitriol) increases tloc(a(CHEBI:"amyloid-beta polypeptide 40"), fromLoc(MESH:Brain), toLoc(MESH:Blood)) View Subject | View Object

1,25(OH)2D3, the active form of vitamin D, plays a key role in enhancing transport of Aβ1–40 from the brain to the blood by reducing RAGE levels at the BBB, and also in contributing to periphery clearance by increasing levels of LRP1 both in vivo and in vitro (Guo et al. 2016b) PubMed:29626319

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a(MESH:"Gastrointestinal Tract") decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

By measuring Aβ levels in superior vena cava and inferior vena cava, it is clear thatAβ levels are getting lower and lower along the direction of the vein blood flow, and the contents of Aβ40 and total Aβ in artery are significantly less than those in vein, suggesting a part of Aβ40 and total Aβ can be cleared by peripheral organs and tissues, such as the liver, kidney, skin, and the gastrointestinal tract, although there is no change in Aβ42 concentrations (Xiang et al. 2015) PubMed:29626319

Appears in Networks:
Annotations
MeSH
Arteries

a(MESH:Kidney) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

By measuring Aβ levels in superior vena cava and inferior vena cava, it is clear thatAβ levels are getting lower and lower along the direction of the vein blood flow, and the contents of Aβ40 and total Aβ in artery are significantly less than those in vein, suggesting a part of Aβ40 and total Aβ can be cleared by peripheral organs and tissues, such as the liver, kidney, skin, and the gastrointestinal tract, although there is no change in Aβ42 concentrations (Xiang et al. 2015) PubMed:29626319

Appears in Networks:
Annotations
MeSH
Arteries

a(MESH:Liver) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

By measuring Aβ levels in superior vena cava and inferior vena cava, it is clear thatAβ levels are getting lower and lower along the direction of the vein blood flow, and the contents of Aβ40 and total Aβ in artery are significantly less than those in vein, suggesting a part of Aβ40 and total Aβ can be cleared by peripheral organs and tissues, such as the liver, kidney, skin, and the gastrointestinal tract, although there is no change in Aβ42 concentrations (Xiang et al. 2015) PubMed:29626319

Appears in Networks:
Annotations
MeSH
Arteries

a(MESH:tenuigenin) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

Tenuigenin could obviously reduce intracerebral Aβ1–40 accumulation in AD mouse brain by increasing the content of 26S proteasome (Chen et al. 2015) PubMed:29626319

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a(MESH:Skin) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

By measuring Aβ levels in superior vena cava and inferior vena cava, it is clear thatAβ levels are getting lower and lower along the direction of the vein blood flow, and the contents of Aβ40 and total Aβ in artery are significantly less than those in vein, suggesting a part of Aβ40 and total Aβ can be cleared by peripheral organs and tissues, such as the liver, kidney, skin, and the gastrointestinal tract, although there is no change in Aβ42 concentrations (Xiang et al. 2015) PubMed:29626319

Appears in Networks:
Annotations
MeSH
Arteries

a(CHEBI:Anatabine) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

Anatabine dose dependently inhibited Aβ1–40 and Aβ1–42 with an approximate half maximal inhibitory concentration of 640 μg/ml for both Aβ1–40 and Aβ1–42 (Fig. 2). PubMed:21958873

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
CHO cell

a(CHEBI:Anatabine) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

We then tested the impact of anatabine on sAPPα and sAPPβ production using 7W CHO cells and observed that anatabine inhibits sAPPβ secretion without impacting sAPPα suggesting that anatabine is preventing the β-cleavage of APP (Fig. 4). PubMed:21958873

Appears in Networks:
Annotations
Experimental Factor Ontology (EFO)
CHO cell

a(CHEBI:Anatabine) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

A significant reduction in the accumulation of brain soluble and insoluble Aβ1–40 and Aβ1–42 was observed following four days of treatment with 2 mg/kg of anatabine (Fig. 9). PubMed:21958873

Appears in Networks:
Annotations
MeSH
Brain

a(CHEBI:"2-[[7-(3,4-dimethoxyphenyl)-5-imidazo[1,2-c]pyrimidinyl]amino]-3-pyridinecarboxamide") decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

We observed that BAY61-3606 significantly reduces brain Aβ38, Aβ40, and Aβ42 levels in Tg PS1/ APPsw mice (Fig. 7, C and D). PubMed:25331948

Appears in Networks:
Annotations
MeSH
Brain

a(CHEBI:Anatabine) decreases a(CHEBI:"amyloid-beta polypeptide 40") View Subject | View Object

It con-siderably lowered the expression of A 1-40 and A 1-42 in an AD transgenic mouse [195]. PubMed:29179999

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

Out-Edges 5

a(CHEBI:"amyloid-beta polypeptide 40") decreases act(a(HBP:"alpha-4 beta-2 nAChR")) View Subject | View Object

Experiments performed on X. laevis oocytes transiently transfected with alpha7 or alpha4beta2 cDNA showed a concentration dependent effect of Abeta on receptor inhibition. In this case the peptide used was Abeta1-40 and the concentrations adopted were between 0.1 and 10 mM, with increased Abeta concentration resulting in a bigger inhibition of the receptor (Tozaki et al., 2002) PubMed:25514383

Appears in Networks:
Annotations
Cell Ontology (CL)
oocyte

a(CHEBI:"amyloid-beta polypeptide 40") decreases act(a(MESH:"alpha7 Nicotinic Acetylcholine Receptor")) View Subject | View Object

Experiments performed on X. laevis oocytes transiently transfected with alpha7 or alpha4beta2 cDNA showed a concentration dependent effect of Abeta on receptor inhibition. In this case the peptide used was Abeta1-40 and the concentrations adopted were between 0.1 and 10 mM, with increased Abeta concentration resulting in a bigger inhibition of the receptor (Tozaki et al., 2002) PubMed:25514383

Appears in Networks:
Annotations
Cell Ontology (CL)
oocyte

a(CHEBI:"amyloid-beta polypeptide 40") increases a(HBP:"amyloid-beta fibrils") View Subject | View Object

Concomitant cleavage of APP by beta and gamma secretase at specific sites can result in fragments (Abeta1-40 or Abeta1-42) that can misfold and form extracellular fibrils. PubMed:14556719

Appears in Networks:

a(CHEBI:"amyloid-beta polypeptide 40") association path(MESH:"Alzheimer Disease") View Subject | View Object

Given the size of AD-related proteins, mono- meric Aβ1-40, Aβ1-42 and tau, should be able to pass freely through astrocytic endfeet clefts at the glial barrier.72 PubMed:26195256

Appears in Networks:

a(CHEBI:"amyloid-beta polypeptide 40") isA a(CHEBI:"amyloid-beta") View Subject | View Object

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.