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Entity

Name
calcium ion homeostasis
Namespace
go
Namespace Version
20181221
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/73688d6dc24e309fca59a1340dc9ee971e9f3baa/external/go-names.belns

Appears in Networks 5

In-Edges 6

p(HGNC:APP) association bp(GO:"calcium ion homeostasis") View Subject | View Object

A role for APP has been suggested in neurite outgrowth and synaptogenesis, neuronal protein trafficking along the axon, transmembrane signal transduction, cell adhesion, calcium metabolism, etc, all requiring additional in vivo evidence (reviewed in [19]) PubMed:21214928

Annotations
Confidence
High

p(HBP:HBP00071) regulates bp(GO:"calcium ion homeostasis") View Subject | View Object

In addition, cellular Ca2+ homeostasis appears to be modulated by AICD (Hamid et al. 2007) PubMed:22122372

p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits") association bp(GO:"calcium ion homeostasis") View Subject | View Object

Recent research interest has focused on the role of calcium dyshomeostasis in AD (Green and LaFerla, 2008); for instance, genetic links with the regulation of cytosolic calcium have been identified (Dreses- Werringloer et al., 2008). Thus nAChRs may provide a link between Abeta and disruption of calcium homeostasis. PubMed:19293145

p(HGNC:PSEN1) association bp(GO:"calcium ion homeostasis") View Subject | View Object

Furthermore, presenilin-1, the most common mutation associated with early-onset familial AD (FAD), plays an essential role in calcium homeostasis and maintaining acidic lysosomal pH, with FAD-associated mutations disrupting calcium-dependent vATPase function in lysosomes [7,18–20] PubMed:29758300

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

Amyloid-β induced apoptosis has also been ascribed to dyshomeostasis of intracellular Ca2+ and oxidative stress [106-108], two critical biochemical derangements known to activate NF-κB PubMed:28745240

act(complex(GO:"NF-kappaB complex")) decreases bp(GO:"calcium ion homeostasis") View Subject | View Object

The three well characterized sensors of intracellular calcium – calmodulin/CamKII pathway, PI3K/ Akt pathway, and protein kinase C (PKC) pathway – are known to induce NF-κB activation and couple upstream signal transduction pathways that induce calcium dyshomeostasis to NF-κB activation PubMed:28745240

Out-Edges 4

bp(GO:"calcium ion homeostasis") association p(HGNC:APP) View Subject | View Object

A role for APP has been suggested in neurite outgrowth and synaptogenesis, neuronal protein trafficking along the axon, transmembrane signal transduction, cell adhesion, calcium metabolism, etc, all requiring additional in vivo evidence (reviewed in [19]) PubMed:21214928

Annotations
Confidence
High

bp(GO:"calcium ion homeostasis") association p(HGNCGENEFAMILY:"Cholinergic receptors nicotinic subunits") View Subject | View Object

Recent research interest has focused on the role of calcium dyshomeostasis in AD (Green and LaFerla, 2008); for instance, genetic links with the regulation of cytosolic calcium have been identified (Dreses- Werringloer et al., 2008). Thus nAChRs may provide a link between Abeta and disruption of calcium homeostasis. PubMed:19293145

bp(GO:"calcium ion homeostasis") association p(HGNC:PSEN1) View Subject | View Object

Furthermore, presenilin-1, the most common mutation associated with early-onset familial AD (FAD), plays an essential role in calcium homeostasis and maintaining acidic lysosomal pH, with FAD-associated mutations disrupting calcium-dependent vATPase function in lysosomes [7,18–20] PubMed:29758300

bp(GO:"calcium ion homeostasis") increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

Amyloid-β induced apoptosis has also been ascribed to dyshomeostasis of intracellular Ca2+ and oxidative stress [106-108], two critical biochemical derangements known to activate NF-κB PubMed:28745240

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.