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

Appears in Networks 3

In-Edges 15

a(CHEBI:"amyloid-beta") increases bp(HBP:HBP00061) View Subject | View Object

Aβ synaptoxicity is Dkk1-dependent12,24 and also appears to be APP-dependent25. PubMed:30232325

p(HGNC:APP) increases bp(HBP:HBP00061) View Subject | View Object

Aβ synaptoxicity is Dkk1-dependent12,24 and also appears to be APP-dependent25. PubMed:30232325

p(HGNC:DKK1) increases bp(HBP:HBP00061) View Subject | View Object

Aβ synaptoxicity is Dkk1-dependent12,24 and also appears to be APP-dependent25. PubMed:30232325

a(CHEBI:"amyloid-beta") increases bp(HBP:HBP00061) View Subject | View Object

While Abeta is neurotoxic, studies suggest that sAPPalpha is neuroprotective, making the subcellular distribution of APP an important factor in neurodegeneration [42-44] PubMed:21214928

Annotations
Confidence
Medium
MeSH
Neurons

a(HBP:HBP00067) decreases bp(HBP:HBP00061) View Subject | View Object

While Abeta is neurotoxic, studies suggest that sAPPalpha is neuroprotective, making the subcellular distribution of APP an important factor in neurodegeneration [42-44] PubMed:21214928

Annotations
Confidence
Medium
MeSH
Neurons

complex(a(CHEBI:"amyloid-beta"), p(HGNC:DNM1)) decreases bp(HBP:HBP00061) View Subject | View Object

Inhibition of dynamin-mediated but not clathrin-mediated Abeta internalization was also found to reduce Abeta-induced neurotoxicity [154] PubMed:21214928

complex(a(HBP:HBP00069), p(HGNC:APP)) increases bp(HBP:HBP00061) View Subject | View Object

One possible mechanism for C31’s toxicity is that C31 complexes with APP to recruit the interacting partners that initiate the signals related to cellular toxicity [136] PubMed:21214928

Annotations
MeSH
Endosomes
Confidence
High
MeSH
Neurons

a(CHEBI:"amyloid-beta") increases bp(HBP:HBP00061) View Subject | View Object

Studies have demonstrated that Abeta overproduction leads to neurotoxicity, neuronal tangle formation, synaptic damage and eventually neuron loss in the pathologically affected brain regions (Selkoe 1998; Shankar and Walsh 2009) PubMed:22122372

a(CHEBI:"amyloid-beta") increases bp(HBP:HBP00061) View Subject | View Object

Although excessive Abeta causes neurotoxicity, some studies have shown that Abeta 40 protects neurons against Abeta 42- induced neuronal damage and is required for the viability of central neurons (Plant et al. 2003; Zou et al. 2003) PubMed:22122372

a(HBP:HBP00042) increases bp(HBP:HBP00061) View Subject | View Object

Although there are only 17 amino acids difference between sAPP-beta and sAPP-alpha, sAPP-beta reportedly lacks most of the neuroprotective effects of sAPP-a (Furukawa et al. 1996a,b) PubMed:22122372

a(HBP:HBP00067) decreases bp(HBP:HBP00061) View Subject | View Object

APP can also be cleaved by alpha-secretase to form a soluble or secreted APP ectodomain (sAPP-alpha) that has been shown to be mostly neuro-protective PubMed:22122372

sec(a(HBP:HBP00067)) decreases bp(HBP:HBP00061) View Subject | View Object

The constitutively secreted sAPP-alpha has been found to be neuro-protective (Mattson et al. 1993; Furukawa et al. 1996a,b; Han et al. 2005; Ma et al. 2009) PubMed:22122372

a(HBP:HBP00069) increases bp(HBP:HBP00061) View Subject | View Object

Caspase-cleavages of APP are thought to be harmful because both C31 and the Jcasp fragment generated were found to be cytotoxic (Lu et al. 2003a) PubMed:22122372

a(HBP:HBP00070) increases bp(HBP:HBP00061) View Subject | View Object

Caspase-cleavages of APP are thought to be harmful because both C31 and the Jcasp fragment generated were found to be cytotoxic (Lu et al. 2003a) PubMed:22122372

p(HGNC:APP, frag("672_711")) decreases bp(HBP:HBP00061) View Subject | View Object

Although excessive Abeta causes neurotoxicity, some studies have shown that Abeta 40 protects neurons against Abeta 42- induced neuronal damage and is required for the viability of central neurons (Plant et al. 2003; Zou et al. 2003) PubMed:22122372

Out-Edges 0

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.