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Entity

Name
neuron cellular homeostasis
Namespace
go
Namespace Version
20180921
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/go-names.belns

Appears in Networks 4

In-Edges 7

a(HBP:HBP00018) decreases bp(GO:"neuron cellular homeostasis") View Subject | View Object

Extracellular deposition of amyloid-β aggregates, the main constituent of senile plaques, is considered to be a pathological hallmark of Alzheimer’s disease that contributes to neuronal dysfunction and behavioural changes PubMed:30046111

a(CHEBI:"amyloid-beta") decreases bp(GO:"neuron cellular homeostasis") View Subject | View Object

It was then postulated that Abeta-nAChR interaction has a physiological role in neuronal homeostasis that is disrupted when Abeta concentrations increase in a pathological context, leading to receptor inhibition and possible cellular toxicity (Dineley et al., 2001; Parri et al., 2011) PubMed:25514383

a(HBP:"4-OH-GTS-21") causesNoChange bp(GO:"neuron cellular homeostasis") View Subject | View Object

Whilst the spatial memory deficit was restored by 4OH-GTS-21 treatment, this molecule had no effect on neuronal density (Ren et al., 2007) PubMed:25514383

a(MESH:"alpha7 Nicotinic Acetylcholine Receptor") regulates bp(GO:"neuron cellular homeostasis") View Subject | View Object

alpha7 nAChR on presynaptic terminals mediate release of others neurotransmitters (Wonnacott et al., 2006), while a postsynaptic or somatic localization elicits important changes in intracellular Ca++ concentration, that can activate second messenger pathways mediating cellular processes such as neuronal survival and gene expression (Berg and Conroy, 2002; Messi et al., 1997; Morley and Happe, 2000) PubMed:25514383

complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) association bp(GO:"neuron cellular homeostasis") View Subject | View Object

It was then postulated that Abeta-nAChR interaction has a physiological role in neuronal homeostasis that is disrupted when Abeta concentrations increase in a pathological context, leading to receptor inhibition and possible cellular toxicity (Dineley et al., 2001; Parri et al., 2011) PubMed:25514383

p(MESH:Proteins, pmod(HBP:misfolding)) decreases bp(GO:"neuron cellular homeostasis") View Subject | View Object

Accumulation of misfolded proteins and damaged organelles is highly detrimental for neuronal homeostasis and survival. PubMed:29758300

bp(GO:autophagy) regulates bp(GO:"neuron cellular homeostasis") View Subject | View Object

It is becoming increasingly evident that the autophagy-lysosomal system is essential to neuronal homeostasis, and may in some settings be neuroprotective PubMed:18930136

Out-Edges 1

bp(GO:"neuron cellular homeostasis") association complex(a(CHEBI:"amyloid-beta"), p(FPLX:CHRN)) View Subject | View Object

It was then postulated that Abeta-nAChR interaction has a physiological role in neuronal homeostasis that is disrupted when Abeta concentrations increase in a pathological context, leading to receptor inhibition and possible cellular toxicity (Dineley et al., 2001; Parri et al., 2011) PubMed:25514383

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.