1. Catalog
  2. Nodes
  3. complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7))

complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7))

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

Components

Appears in Networks 4

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

Cholinergic system during the progression of Alzheimer’s disease: therapeutic implications v1.0.0

Chaperoning α7 neuronal nicotinic acetylcholine receptors v1.0.0

In-Edges 4

a(MESH:Bungarotoxins) decreases complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) View Subject | View Object

It is noteworthy that this internalization was blocked by alpha-bungarotoxin, which may indicate that alpha-bungarotoxin either inhibits binding of Abeta to the alpha7 receptor (and therefore that Abeta toxicity results from binding of Abeta to alpha7 nAChRs) or directly inhibits alpha7 nAChR internalization. PubMed:19293145

Appears in Networks:

complex(a(MESH:Bungarotoxins), p(HGNC:CHRNA7)) decreases complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) View Subject | View Object

One study showed high-affinity binding of Abeta at picomolar levels to human alpha7 nAChRs heterologously expressed in cell lines, based both on the ability of Abeta to displace labeled alpha-bungarotoxin and the ability of alpha-bungarotoxin to displace fluorescently labeled Abeta (Wang et al., 2000b). PubMed:19293145

Appears in Networks:

complex(a(MESH:Bungarotoxins), p(HGNC:CHRNA7)) decreases complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) View Subject | View Object

In contrast, Small et al. (2007) found no displacement of alpha-BTX from SH-SY5Y cells (a cell line very closely related to that used by Wang et al.) by either amyloid or methyllycaconitine. Wang et al. (2000b) also showed similar staining of human AD cortical neurons by alpha7 and Abeta antibodies in double immunofluorescence, suggesting that in human cortical neurons, alpha7 and Abeta are closely associated, although such an approach does not prove direct binding. However another study (Small et al., 2007) showed no displacement of labeled alpha-bungarotoxin from cell lines expressing rat alpha7 nAChRs. PubMed:19293145

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

p(HGNC:CHRNA7) increases complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) View Subject | View Object

Despite a putative beneficial role for increased CBF neuron alpha7 nAChR expression in AD (that may also be relevant to smoking behavior), evidence suggests that increased alpha7 nAChR expression contributes to cellular degeneration. Notably, alpha7 nAChR binds and/or interacts with APP and Ab peptides [123–125]. Increased NB neuronal alpha7 nAChR expression may arise as a compensatory response that is offset by aberrant Ab-alpha7 nAChR interactions, leading to cholinergic dysfunction. PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Cognitive Dysfunction

Out-Edges 8

complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) hasComponent a(CHEBI:"amyloid-beta") View Subject | View Object

Appears in Networks:

complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) hasComponent p(HGNC:CHRNA7) View Subject | View Object

Appears in Networks:

complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) increases path(HBP:neurotoxicity) View Subject | View Object

Paradoxically, in addition to their neuroprotective action, nAChRs may also partly mediate the toxic action of Abeta. The toxicity of Abeta on SH-SY5Y cells, as measured by a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, in which the health of cells is monitored by their ability of cells to reduce 3-(4,5-dimethylthiazol- 2-yl)-2,5-diphenyltetrazolium bromide, was significantly impaired when alpha7 was silenced by RNAi, suggesting that Abeta may exert its toxicity, at least in part, through a pathway that includes alpha7 nAChRs (Qi et al., 2007). PubMed:19293145

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

complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) decreases complex(a(MESH:Bungarotoxins), p(HGNC:CHRNA7)) View Subject | View Object

One study showed high-affinity binding of Abeta at picomolar levels to human alpha7 nAChRs heterologously expressed in cell lines, based both on the ability of Abeta to displace labeled alpha-bungarotoxin and the ability of alpha-bungarotoxin to displace fluorescently labeled Abeta (Wang et al., 2000b). PubMed:19293145

Appears in Networks:

complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) increases r(HGNC:CHRNA7) View Subject | View Object

Despite a putative beneficial role for increased CBF neuron alpha7 nAChR expression in AD (that may also be relevant to smoking behavior), evidence suggests that increased alpha7 nAChR expression contributes to cellular degeneration. Notably, alpha7 nAChR binds and/or interacts with APP and Ab peptides [123–125]. Increased NB neuronal alpha7 nAChR expression may arise as a compensatory response that is offset by aberrant Ab-alpha7 nAChR interactions, leading to cholinergic dysfunction. PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Cognitive Dysfunction

complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) decreases bp(GO:"GO:0007271") View Subject | View Object

Despite a putative beneficial role for increased CBF neuron alpha7 nAChR expression in AD (that may also be relevant to smoking behavior), evidence suggests that increased alpha7 nAChR expression contributes to cellular degeneration. Notably, alpha7 nAChR binds and/or interacts with APP and Ab peptides [123–125]. Increased NB neuronal alpha7 nAChR expression may arise as a compensatory response that is offset by aberrant Ab-alpha7 nAChR interactions, leading to cholinergic dysfunction. PubMed:18986241

Appears in Networks:
Annotations
Disease Ontology (DO)
Alzheimer's disease
MeSH
Cognitive Dysfunction

complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) increases bp(GO:"neuron death") View Subject | View Object

Another important event that associates well with the Alzheimer disease pathology is the aggregation of the β-amyloid peptide [53]. This peptide interacts with α7 AChRs and has been reported to affect the nor- mal functioning of the latter, causing reduced neuronal survival [146,192–194]. PubMed:22040696

Appears in Networks:
Annotations
MeSH
Hippocampus

complex(a(CHEBI:"amyloid-beta"), p(HGNC:CHRNA7)) decreases act(p(HGNC:CHRNA7)) View Subject | View Object

Another important event that associates well with the Alzheimer disease pathology is the aggregation of the β-amyloid peptide [53]. This peptide interacts with α7 AChRs and has been reported to affect the nor- mal functioning of the latter, causing reduced neuronal survival [146,192–194]. PubMed:22040696

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.