1. Catalog
  2. Nodes
  3. a(HBP:"amyloid-beta fibrils")

a(HBP:"amyloid-beta fibrils")

Equivalencies: 0 | Classes: 1 | Children: 0 | Explore

Entity

Name
amyloid-beta fibrils
Namespace
HBP
Namespace Version
20181029
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/785431732a26d6809b4162d98b95687d16404e63/export/hbp-names.belns

Appears in Networks 5

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

Alzheimer's Disease: Targeting the Cholinergic System v1.0.0

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

Alzheimer's disease-type neuronal tau hyperphosphorylation induced by A beta oligomers v1.0.0

This document contains the bel code for the Article Alzheimer’s disease-type neuronal tau hyperphosphorylation induced by Abeta oligomers by De Felice et al

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage v1.0.0

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage from Shafiei et al., 2017

In-Edges 5

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

In this work, kinetic analyses revealed that a structural motif in AChE (a hydrophobic sequence of 35 resides peptides) was able to promote amyloid formation and its incorporation into the growing Aβ-fibrils PubMed:26813123

Appears in Networks:

complex(a(MESH:"Amyloid beta-Peptides"), p(HGNC:ACHE)) increases a(HBP:"amyloid-beta fibrils") View Subject | View Object

A molecular modeling study showed that AChE interacts with the Aβ peptide and promotes amyloid fibril formation PubMed:26813123

Appears in Networks:

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 42") 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(MESH:"Heparan Sulfate Proteoglycans") increases a(HBP:"amyloid-beta fibrils") View Subject | View Object

Consistently, HSPGs have been implicated in amyloid as well as tau fibril formation in vitro, presumably facilitated by anionic moieties PubMed:28420982

Appears in Networks:
Annotations
MeSH
Extracellular Space
Confidence
High
MeSH
Exosomes
MeSH
Alzheimer Disease

Out-Edges 7

a(HBP:"amyloid-beta fibrils") isA a(CHEBI:"amyloid-beta") View Subject | View Object

Appears in Networks:

a(HBP:"amyloid-beta fibrils") increases p(HGNC:MAPT, pmod(Ph)) View Subject | View Object

Hippocampal neurons exposed to Abeta fibrils rather than oligomers also showed elevated P-tau immunofluorescence (Fig. 2N–P) However, although fibrils could be seen attached to neurons, they did not bind in the synaptic pattern observed for ADDLs (Fig. 2O and P). PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

a(HBP:"amyloid-beta fibrils") increases p(HGNC:MAPT, pmod(Ph, Thr, 231)) View Subject | View Object

Vehicle-treated neurons (Fig. 3A and E) exhibited very low phosphotau immunofluorescence, but neurons treated for 4 h with 500nM ADDLs showed significantly higher levels in immunofluorescence of P-Ser404 and P-Thr231 tau (Fig. 3B and F, respectively). Neurons treated for 4 h with 10M Abeta fibrils also showed an increase in immunofluorescence of P-Ser404 and P-Thr231 tau (Fig. 3C and G, respectively). PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

a(HBP:"amyloid-beta fibrils") increases p(HGNC:MAPT, pmod(Ph, Thr, 231)) View Subject | View Object

Verification of the findings from immunofluorescence microscopy was provided by Western blot analysis of hippocampal neuronal lysates with P404, P231 and P181 antiphosphotau antibodies. A 4 h exposure to 500nM ADDLs resulted in a significant increase in tau phosphorylated at the three epitopes, to levels similar to those observed after exposure to 10 M Abeta fibrils (Fig. 4A–D). PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

a(HBP:"amyloid-beta fibrils") increases p(HGNC:MAPT, pmod(Ph, Ser, 404)) View Subject | View Object

Vehicle-treated neurons (Fig. 3A and E) exhibited very low phosphotau immunofluorescence, but neurons treated for 4 h with 500nM ADDLs showed significantly higher levels in immunofluorescence of P-Ser404 and P-Thr231 tau (Fig. 3B and F, respectively). Neurons treated for 4 h with 10M Abeta fibrils also showed an increase in immunofluorescence of P-Ser404 and P-Thr231 tau (Fig. 3C and G, respectively). PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

a(HBP:"amyloid-beta fibrils") increases p(HGNC:MAPT, pmod(Ph, Ser, 404)) View Subject | View Object

Verification of the findings from immunofluorescence microscopy was provided by Western blot analysis of hippocampal neuronal lysates with P404, P231 and P181 antiphosphotau antibodies. A 4 h exposure to 500nM ADDLs resulted in a significant increase in tau phosphorylated at the three epitopes, to levels similar to those observed after exposure to 10 M Abeta fibrils (Fig. 4A–D). PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

a(HBP:"amyloid-beta fibrils") increases p(HGNC:MAPT, pmod(Ph, Thr, 181)) View Subject | View Object

Verification of the findings from immunofluorescence microscopy was provided by Western blot analysis of hippocampal neuronal lysates with P404, P231 and P181 antiphosphotau antibodies. A 4 h exposure to 500nM ADDLs resulted in a significant increase in tau phosphorylated at the three epitopes, to levels similar to those observed after exposure to 10 M Abeta fibrils (Fig. 4A–D). PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

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.