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a(GO:axon)

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Entity

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

Appears in Networks 3

Amelioration of Experimental Autoimmune Encephalomyelitis by Anatabine v1.0.0

Tau Modifications v1.9.5

Tau Modifications Sections of NESTOR

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

In-Edges 8

act(p(HGNC:DYRK1A)) regulates a(GO:axon) View Subject | View Object

We conclude that the Dyrk1a dosage is critical for proper neurite and axonal outgrowth and that the two nonsense mutations, R205X and E239X, are loss-of-function mutants. PubMed:28167836

Appears in Networks:

bp(GO:"axon guidance") increases a(GO:axon) View Subject | View Object

NF-κB also plays a vital role in axon guidance subsequent to neurogenesis and axon growth in response to neurotrophins, resulting in the integration of the nascent neurons PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

act(complex(GO:"NF-kappaB complex")) increases a(GO:axon) View Subject | View Object

Multiple studies have implicated NF-κB in the regulation of post-natal axonal growth or neurite outgrowth. PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:GFRA1) increases a(GO:axon) View Subject | View Object

Furthermore, NF-κB directly regulates the expression of a plethora of cell adhesion molecules such as neural cell adhesion molecule (NCAM) [202], slit and Trk-like family member 1 (SLITRK1) [203], glial cell-derived neurotrophic factor receptor α1 (GFRα1) [204], and T-lymphoma and metastasis 1 (TLAM1) [203], key players in directing axon growth. PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:ITGB1) increases a(GO:axon) View Subject | View Object

NF-κB positively regulates the expression of extracellular matrix protein involved in cell adhesion, β1-integrin [199], a well characterized pivotal player in axon growth initiation and guidance PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:NCAM1) increases a(GO:axon) View Subject | View Object

Furthermore, NF-κB directly regulates the expression of a plethora of cell adhesion molecules such as neural cell adhesion molecule (NCAM) [202], slit and Trk-like family member 1 (SLITRK1) [203], glial cell-derived neurotrophic factor receptor α1 (GFRα1) [204], and T-lymphoma and metastasis 1 (TLAM1) [203], key players in directing axon growth. PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:SLITRK1) increases a(GO:axon) View Subject | View Object

Furthermore, NF-κB directly regulates the expression of a plethora of cell adhesion molecules such as neural cell adhesion molecule (NCAM) [202], slit and Trk-like family member 1 (SLITRK1) [203], glial cell-derived neurotrophic factor receptor α1 (GFRα1) [204], and T-lymphoma and metastasis 1 (TLAM1) [203], key players in directing axon growth. PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

p(HGNC:TIAM1) increases a(GO:axon) View Subject | View Object

Furthermore, NF-κB directly regulates the expression of a plethora of cell adhesion molecules such as neural cell adhesion molecule (NCAM) [202], slit and Trk-like family member 1 (SLITRK1) [203], glial cell-derived neurotrophic factor receptor α1 (GFRα1) [204], and T-lymphoma and metastasis 1 (TLAM1) [203], key players in directing axon growth. PubMed:28745240

Appears in Networks:
Annotations
MeSH
Alzheimer Disease

Out-Edges 2

act(a(GO:axon)) decreases path(MESH:Paralysis) View Subject | View Object

The axonal damage in EAE mice leads to well defined clinical signs such as tail paralysis, hind-limb weakness and paralysis PubMed:23383175

Appears in Networks:
Annotations
MeSH
Encephalomyelitis

act(a(GO:axon)) decreases path(HP:"Limb muscle weakness") View Subject | View Object

The axonal damage in EAE mice leads to well defined clinical signs such as tail paralysis, hind-limb weakness and paralysis PubMed:23383175

Appears in Networks:
Annotations
MeSH
Encephalomyelitis

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.