1. Catalog
  2. Namespaces
  3. Cell Ontology (CL)
  4. motor neuron

motor neuron

Name
motor neuron
Namespace Keyword
Cell
Namespace
Cell Ontology (CL)
Namespace Version
20170511
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/annotation/cell/cell-20170511.belanno

Sample Annotated Edges 5

bp(HBP:Proteostasis) decreases bp(MESH:Aging) View Subject | View Object

As such, it is feasible that any reduction in the protein degradation capacity of a cell could contribute to proteostasis collapse and promote aging. PubMed:25784053

Appears in Networks:
Annotations
Cell Ontology (CL)
motor neuron

a(PUBCHEM:10521421) increases bp(GO:autophagy) View Subject | View Object

An in silico screen based on the structure of 10-NCP, an Akt inhibitor that potently induces autophagy (144), identified the molecules FPZ and MTM as potent activators of autophagic flux and clearance of TDP-43 in mammalian cells (145). PubMed:25784053

Appears in Networks:
Annotations
Cell Ontology (CL)
motor neuron

bp(MESH:Aging) decreases p(FPLX:HSP90) View Subject | View Object

Additionally, an investigation of chaperone and cochaperone gene expression in young (36±4 years of age) and aged (73 ±4 years of age) human brain tissue revealed that of 332 genes examined, 101 are significantly repressed with age, including HSP70, HSP40, HSP90, and TRiC genes (113). Furthermore, 62 chaperone genes, including several small HSPs, were found to be significantly induced, likely as a result of the cellular response to accumulating protein damage with age (113). PubMed:25784053

Appears in Networks:
Annotations
Cell Ontology (CL)
motor neuron

path(MESH:"Amyotrophic Lateral Sclerosis") negativeCorrelation p(HGNC:ATF6) View Subject | View Object

Disruption of the ATF6 arm of the UPR(ER) is reported to occur in mouse models of HD and a VAPB cell model of ALS, suggesting that differential changes in UPR arms may be a feature of disease progression (102, 103). PubMed:25784053

Appears in Networks:
Annotations
Cell Ontology (CL)
motor neuron

act(p(FPLX:HSP90)) decreases act(p(HGNC:HSF1)) View Subject | View Object

One strategy is to directly activate HSF1, thereby increasing the expression of multiple molecular chaperones simultaneously. This approach has been traditionally achieved by inhibition of HSP90 with compounds that bind the N-terminal ATP-binding pocket, such as radicicol, geldanamycin, or 17-AAG (64, 132–134). PubMed:25784053

Appears in Networks:
Annotations
Cell Ontology (CL)
motor neuron

Showing 5 of 60 edges

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.