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Lysosomes

Name
Lysosomes
Namespace Keyword
MeSHAnatomy
Namespace
MeSH
Namespace Version
20170511
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/annotation/mesh-anatomy/mesh-anatomy-20170511.belanno

Sample Annotated Edges 5

a(CHEBI:cilostazol) increases p(HGNC:CTSB) View Subject | View Object

Cilostazol (a phosphodiesterase 3 inhibitor) clears Aβ42 from neuronal cell lines by promoting autophagy, upregulating beclin 1, ATG5 and LC3, downregulating mTORC1 and inducing lysosomal cathepsin B; these actions of cilostazol involve activation of SIRT1 as well as upstream Tyr172 phosphorylation of AMPK 108,162,163 . PubMed:30116051

Appears in Networks:
Annotations
MeSH
Lysosomes
MeSH
Machado-Joseph Disease

p(HGNC:PSEN1) increases p(HGNC:ATP6V0A1, pmod(NGlyco)) View Subject | View Object

In the absence of PS1, the V0a1 subunit of v-ATPase is not N-glycosylated in the ER and is degraded before sufficient amounts can be delivered to autolysosomes/lysosomes to support lysosomal acidification. PubMed:22908190

Appears in Networks:
Annotations
MeSH
Lysosomes

p(HGNC:PSEN1) increases act(a(MESH:Cathepsins)) View Subject | View Object

Beyond its role as a component of g-secretase, Presenilin 1 (PS1) is required for lysosome acidification, which is needed to activate cathepsins and other hydrolases that carry out digestion during autophagy (Lee et al. 2010). PubMed:22908190

Appears in Networks:
Annotations
MeSH
Lysosomes

p(HGNC:ATP6V0A1, pmod(NGlyco)) increases bp(GO:"pH reduction") View Subject | View Object

In the absence of PS1, the V0a1 subunit of v-ATPase is not N-glycosylated in the ER and is degraded before sufficient amounts can be delivered to autolysosomes/lysosomes to support lysosomal acidification. PubMed:22908190

Appears in Networks:
Annotations
MeSH
Lysosomes

p(HGNC:PSEN1, var("?")) decreases bp(GO:"pH reduction") 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

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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.