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a(MESH:Neurites)

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

Entity

Name
Neurites
Namespace
MeSH
Namespace Version
20181007
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/01c9daa61012b37dd0a1bc962521ba51a15b38f1/external/mesh-names.belns

Appears in Networks 2

The Ubiquitin–Proteasome System and the Autophagic–Lysosomal System in Alzheimer Disease v1.0.0

Tau in physiology and pathology v1.0.0

In-Edges 4

a(HBP:AβOs) increases deg(a(MESH:Neurites)) View Subject | View Object

Recently, it has been shown that soluble Ab oligomers isolated from AD cortex can induce tau hyperphosphorylation at AD-relevant epitopes and subsequent neuritic degeneration (Jin et al. 2011). PubMed:22908190

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:APP, var("?")) negativeCorrelation act(a(MESH:Neurites)) View Subject | View Object

Similar neuritic dystrophy eventually develops in all forms of AD and in mouse AD models where only FAD-causingmutant APP is overexpressed. PubMed:22908190

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:PSEN1, var("?")) decreases act(a(MESH:Neurites)) View Subject | View Object

These observations suggest how PS1 mutations, which impede lysosomal acidification (Lee et al. 2010), may markedly accelerate and amplify neuritic dystrophy in AD PubMed:22908190

Appears in Networks:
Annotations
MeSH
Lysosomes
MeSH
Alzheimer Disease

p(HGNC:MAPT) increases a(MESH:Neurites) View Subject | View Object

In addition, tau seems to be essential for axonal elongation and maturation, as knockdown of tau in cultured rat neurons inhibits neurite formation, whereas overexpression of tau promotes the formation of neurites even in non-neuronal cells1 PubMed:26631930

Appears in Networks:
Annotations
MeSH
Neurons

Out-Edges 1

act(a(MESH:Neurites)) negativeCorrelation p(HGNC:APP, var("?")) View Subject | View Object

Similar neuritic dystrophy eventually develops in all forms of AD and in mouse AD models where only FAD-causingmutant APP is overexpressed. PubMed:22908190

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

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.