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bp(HBP:HBP00037)

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Entity

Name
HBP00037
Namespace
HBP
Namespace Version
20181029
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/785431732a26d6809b4162d98b95687d16404e63/export/hbp.belns

Appears in Networks 4

Amyloid β oligomers (AβOs) in Alzheimer’s disease v1.0.0

Alpha-synuclein oligomers: a new hope v1.0.0

MMP-9 and MMP-2 Contribute to Neuronal Cell Death in iPSC Models of Frontotemporal Dementia with MAPT Mutations v1.0.0

Tau protein aggregation is associated with cellular senescence in the brain v1.0.0

In-Edges 4

act(p(HGNC:GRIN1)) increases bp(HBP:HBP00037) View Subject | View Object

Excessive activation of NMDAR by soluble AβOs triggers disproportionate influx of Ca2+ into neurons, which leads to excitotoxicity, mitochondrial dysfunction, and loss of synapses (Zhao et al. 2004). PubMed:29196815

Appears in Networks:
Annotations
MeSH
Extracellular Space
Cell Ontology (CL)
neuron
Confidence
Medium

a(HBP:HBP00093) increases bp(HBP:HBP00037) View Subject | View Object

All these results show that a-syn oligomers are implicated in mitochondrial dysfunction across different models. PubMed:28803412

Appears in Networks:
Annotations
Confidence
High

a(CHEBI:rotenone) increases bp(HBP:HBP00037) View Subject | View Object

We treated these neurons with staurosporine, a broad-spectrum kinase inhibitor that induces apoptosis (Budd et al., 2000); rotenone, a complex inhibitor that induces mitochondrial dysfunction (Sherer et al., 2003); and rapamycin, an inhibitor of the mammalian target of the rapamycin (mTOR) signaling pathway with many downstream effects (Li et al., 2014) PubMed:27594586

Appears in Networks:
Annotations
MeSH
Extracellular Space
Confidence
High
MeSH
Cerebral Cortex
MeSH
Neurons
MeSH
Frontotemporal Dementia

bp(GO:"cellular senescence") increases bp(HBP:HBP00037) View Subject | View Object

Mitochondrial dysfunction is obligatory for SASP production and cellular senescence (Correia-Melo et al., 2016; Hutter et al., 2004) PubMed:30126037

Appears in Networks:
Annotations
Confidence
High
MeSH
Neurons
MeSH
Alzheimer Disease

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.