1. Catalog
  2. Nodes
  3. a(HBP:"amyloid-beta derived diffusible ligands")

a(HBP:"amyloid-beta derived diffusible ligands")

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

Entity

Name
amyloid-beta derived diffusible ligands
Namespace
HBP
Namespace Version
20190207
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/cf4d8bb88754f036b943b4d94ad96e103dcb7149/export/hbp-names.belns

Appears in Networks 3

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

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

TAU and Interaction Partners v1.2.5

TAU Interactions Section of NESTOR

In-Edges 6

a(HBP:"amyloid-beta antibody, NU1") decreases act(a(HBP:"amyloid-beta derived diffusible ligands")) View Subject | View Object

NU1 completely blocked the increase in P-Ser404 and P-Thr231 phosphotau levels induced by ADDLs (Fig. 3D–H). PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

complex(a(GO:synapse), a(HBP:"amyloid-beta derived diffusible ligands")) hasComponent a(HBP:"amyloid-beta derived diffusible ligands") View Subject | View Object

Appears in Networks:

complex(a(HBP:"amyloid-beta derived diffusible ligands"), a(MESH:Neurons)) hasComponent a(HBP:"amyloid-beta derived diffusible ligands") View Subject | View Object

Appears in Networks:

complex(a(HBP:"amyloid-beta derived diffusible ligands"), p(HGNC:MAPT)) hasComponent a(HBP:"amyloid-beta derived diffusible ligands") View Subject | View Object

Appears in Networks:

bp(GO:"import into cell") decreases a(HBP:"amyloid-beta derived diffusible ligands") View Subject | View Object

Soluble Aβ can be removed from the brain by various clearance systems, including enzymatic degradation and cellular uptake, transport across the blood–brain barrier (BBB) and blood–cerebrospinal fluid barrier (BCSFB), interstitial fluid (ISF) bulk flow, and cerebro- spinal fluid (CSF) absorption into the circulatory and lymphatic systems. PubMed:26195256

Appears in Networks:

act(p(HGNC:BACE1)) increases a(HBP:"amyloid-beta derived diffusible ligands") View Subject | View Object

If APP is first cleaved by β-secretase 1 (also known as BACE1) instead of α-secretase, the subsequent γ-secretase cleavage will result in soluble monomeric Aβ. PubMed:26195256

Appears in Networks:

Out-Edges 12

a(HBP:"amyloid-beta derived diffusible ligands") decreases bp(MESH:"Cell Survival") View Subject | View Object

At longer incubation times (48 and 96 h) ADDLs caused a progressive decrease in MTT reduction (Fig. 1B), which can be due to altered trafficking (Liu et al., 1998) as well as cell death. PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

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

While vehicle treated cells (Fig. 2A and B) exhibited low phosphotau immunofluorescence, cells treated with 1 microM biotinylated ADDLs (bADDLs) for 6 h (Fig. 2C and D) showed a significant increase in P-tau immunofluorescence (Fig. 2D). PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

a(HBP:"amyloid-beta derived diffusible ligands") increases p(RGD:Mapt, pmod(Ph)) View Subject | View Object

We then investigated whether bADDLs also induced tau phosphorylation in rat hippocampal neurons. To this end, we initially used frozen dissociated rat hippocampal cell preparations (Cambrex). Cells were maintained in the presence of 1M bADDLs (Fig. 2I and J) or vehicle (not shown) for 6 h at 37 ◦C. We observed a marked P-tau immunostaining in a subpopulation of neurons that also had ADDLs bound (Fig. 2I, arrowheads), while cells that did not bind bADDLs had no AT8 staining (Fig. 2J). PubMed:17403556

Appears in Networks:
Annotations
MeSH
Hippocampus
Text Location
Results

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

Following exposure to ADDLs, double-label immunofluorescence microscopy showed high levels of tau phosphorylated at Thr231, which discriminates among AD and non-AD subjects and patients with other forms of dementia (Hampel et al., 2004, 2003), in neurons with prominent dendritic ADDL binding (detected with NU1, Fig. 2K–M). ADDL binding to synaptic hot-spots in hippocampal neurons is evident in images at highermagnification (60×objective, PanelsLand M). PubMed:17403556

Appears in Networks:
Annotations
Text Location
Results

a(HBP:"amyloid-beta derived diffusible ligands") 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 derived diffusible ligands") 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 derived diffusible ligands") increases complex(a(GO:synapse), a(HBP:"amyloid-beta derived diffusible ligands")) View Subject | View Object

Following exposure to ADDLs, double-label immunofluorescence microscopy showed high levels of tau phosphorylated at Thr231, which discriminates among AD and non-AD subjects and patients with other forms of dementia (Hampel et al., 2004, 2003), in neurons with prominent dendritic ADDL binding (detected with NU1, Fig. 2K–M). ADDL binding to synaptic hot-spots in hippocampal neurons is evident in images at highermagnification (60×objective, PanelsLand M). PubMed:17403556

Appears in Networks:
Annotations
MeSH
Hippocampus
Text Location
Results

a(HBP:"amyloid-beta derived diffusible ligands") 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 derived diffusible ligands") 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 derived diffusible ligands") 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

a(HBP:"amyloid-beta derived diffusible ligands") increases tloc(p(MGI:Fyn), fromLoc(GO:cytoplasm), toLoc(GO:"membrane raft")) View Subject | View Object

A rapid but transient increase was found in the amount of fyn detected in DRMs on ADDL exposure for 2 min that was partially reduced after 10 min exposure. Mirroring the movement of fyn into the DRM, tau content of DRMs increased in response to ADDLs. To further test a putative association between fyn and tau levels in DRMs, we treated cells with 2-bromopalmitate, an inhibitor of protein palmitoylation, which is required for fyn’s localization in DRMs. This treatment resulted in a progressive reduction in both fyn and tau in DRMs, demonstrating that the association of tau with DRMs may be directly regulated by fyn (Supplemental Fig. 2). PubMed:18096814

Appears in Networks:
Annotations
MeSH
Hippocampus

a(HBP:"amyloid-beta derived diffusible ligands") increases tloc(p(MGI:Mapt), fromLoc(GO:cytoplasm), toLoc(GO:"membrane raft")) View Subject | View Object

A rapid but transient increase was found in the amount of fyn detected in DRMs on ADDL exposure for 2 min that was partially reduced after 10 min exposure. Mirroring the movement of fyn into the DRM, tau content of DRMs increased in response to ADDLs. To further test a putative association between fyn and tau levels in DRMs, we treated cells with 2-bromopalmitate, an inhibitor of protein palmitoylation, which is required for fyn’s localization in DRMs. This treatment resulted in a progressive reduction in both fyn and tau in DRMs, demonstrating that the association of tau with DRMs may be directly regulated by fyn (Supplemental Fig. 2). PubMed:18096814

Appears in Networks:
Annotations
MeSH
Hippocampus

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.